ARTICLE

Functional Significance of Cell Volume Regulatory Mechanisms

1 Institute of Physiology, University of Tübingen, Tübingen; Department of Internal Medicine, University of Düsseldorf, Düsseldorf, Germany; and Department of Internal Medicine and Institute of Physiology, University of Innsbruck, Innsbruck, Austria

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GILLIAN L. BUSCH

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MARKUS RITTER

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HARALD VÖLKL

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SIEGFRIED WALDEGGER

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ERICH GULBINS

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, and

DIETER HÄUSSINGER

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Published Online:01 Jan 1998https://doi.org/10.1152/physrev.1998.78.1.247

Abstract

Lang, Florian, Gillian L. Busch, Markus Ritter, Harald Völkl, Siegfried Waldegger, Erich Gulbins, and Dieter Häussinger. Functional Significance of Cell Volume Regulatory Mechanisms. Physiol. Rev. 78: 247–306, 1998. — To survive, cells have to avoid excessive alterations of cell volume that jeopardize structural integrity and constancy of intracellular milieu. The function of cellular proteins seems specifically sensitive to dilution and concentration, determining the extent of macromolecular crowding. Even at constant extracellular osmolarity, volume constancy of any mammalian cell is permanently challenged by transport of osmotically active substances across the cell membrane and formation or disappearance of cellular osmolarity by metabolism. Thus cell volume constancy requires the continued operation of cell volume regulatory mechanisms, including ion transport across the cell membrane as well as accumulation or disposal of organic osmolytes and metabolites. The various cell volume regulatory mechanisms are triggered by a multitude of intracellular signaling events including alterations of cell membrane potential and of intracellular ion composition, various second messenger cascades, phosphorylation of diverse target proteins, and altered gene expression. Hormones and mediators have been shown to exploit the volume regulatory machinery to exert their effects. Thus cell volume may be considered a second message in the transmission of hormonal signals. Accordingly, alterations of cell volume and volume regulatory mechanisms participate in a wide variety of cellular functions including epithelial transport, metabolism, excitation, hormone release, migration, cell proliferation, and cell death.

I. INTRODUCTION

With only few exceptions (416), the membranes of animal cells are highly permeable to water (212 776). Animal cell membranes cannot tolerate substantial hydrostatic pressure gradients, and water movement across those membranes is in large part dictated by osmotic pressure gradients (406 445 608 985 1043). Thus any imbalance of intracellular and extracellular osmolarity is paralleled by respective water movement across cell membranes and subsequent alterations of cell volume.

As outlined below, most mammalian cells are bathed in extracellular fluid with almost constant osmolarity. Nevertheless, considerable alterations of extracellular osmolarity are encountered in a variety of diseases. Excessive alterations of extracellular osmolarity occur in kidney medulla during transition between antidiuresis and diuresis (63).

Even at constant extracellular osmolarity, cell volume constancy is compromised by alterations of intracellular osmolarity. A wide variety of metabolic pathways leads to cellular formation or dissipation of osmotically active substances. Moreover, transport across the cell membrane modifies cellular osmolarity and thus cell volume.

To avoid excessive alterations of cell volume, cells have developed and utilize a multitude of volume regulatory mechanisms including transport across the cell membrane and metabolism. These mechanisms are triggered by minute alterations of cell volume. They not only serve to readjust cell volume but profoundly modify a wide variety of cellular functions. Thus cell volume is an integral element within the cellular machinery regulating cellular performance.

It is the aim of this review to illustrate the functional significance of cell volume. To this end, a description of the volume regulatory mechanisms and the cellular functions sensitive to cell volume is followed by a discussion of the role of cell volume in several integrated cell functions.

This review does not consider volume regulatory mechanisms in prokaryotic cells or comparative aspects of cell volume regulation, and the reader may refer to the respective pertinent literature (84 96 128 175 225 232 236 309 336 387–391 395 400 604 698 763 792 852 970 1121 1138 1168).

Instead, the discussion focuses on the significance of cell volume for the performance of mammalian cells. Moreover, the paper stresses recent developments. For a more complete coverage of earlier literature, the reader may refer to previous reviews on cell volume regulation (114 425 539 545 682 776 778 815 817 843 911a 971 1061 1168), osmolytes (63 142 144 370), and the role of cell volume in regulation of cell function (495 693).

For various functions, experimental evidence pointing to the involvement of cell volume and cell volume regulatory mechanisms is intriguing but far from conclusive. It is hoped that this review stimulates further experimental effort in this exciting area of research to clarify the many remaining questions.

II. CELL VOLUME REGULATORY MECHANISMS

Rapid changes of cell volume are usually caused by movement of water across the cell membrane (J_v), which is driven by a hydrostatic (Δp) and osmotic (Δπ) pressure gradient and depends on the hydraulic conductivity of the cell membrane (L_p)

J_{v} = L_{p} (Δ p - Δ π)

Δπ depends on the effective concentration difference across the cell membrane (Δc) and the reflection coefficient (σ) for each solute i

Δ π = RT Σ σ_{i} Δ c_{i}

where R and T are the gas constant and the absolute temperature, respectively. Application of the equations would require that the cytosol behaves as a dilute solution. This is not entirely true, as discussed elsewhere in detail (194–196 357 722). The cell membrane does not withstand hydrostatic pressure gradients exceeding 2 kPa (445), which is equivalent to 1 mmol/l Δc. Even though interaction of the cell membrane with the cytoskeleton may allow the hydrostatic gradient to become larger (382 577 828), the movement of water is mainly dictated by osmotic gradients across the cell membrane.

The L_p depends on the presence of water channels (aquaporins) in the cell membrane, a family of molecules, which are inserted into the cell membrane and allow the passage of water (6 214 270 300 349 356 494 536 565 773 980). The aquaporins are especially important in water transporting epithelia but may be expressed in nonepithelial cells. Even though osmotically driven water transport is an obvious requirement for osmotic cell swelling and cell volume regulation, water movement across the cell membrane is rarely a limiting factor in cell volume changes. Thus alterations of intra- or extracellular osmolarity are in general followed by the respective movements of water and alterations of cell volume.

Cell volume regulatory mechanisms are thus most conveniently disclosed by exposing cells to abrupt changes of extracellular osmolarity. If cells are exposed to hypotonic extracellular fluid, they initially swell as more or less perfect osmometers but then approach the original cell volume by so-called regulatory cell volume decrease (RVD). If cells are exposed to hypertonic extracellular fluid, they initially shrink like almost perfect osmometers but then may approach the original cell volume by so-called regulatory cell volume increase (RVI). It should be kept in mind, however, that exposure of cells to anisotonic extracellular fluid does not only modify cell volume but also the volume of intracellular organelles such as mitochondria (969). Furthermore, in parallel to cellular osmolarity, cellular ionic strength is altered even if extracellular ionic strength is kept constant. Thus the sequelae of osmotic alterations of cell volume are not necessarily identical to the consequences of isotonic alterations of cell volume.

Alterations of cell volume may be limited by constraints from extracellular tissue, as shown for the brain (1220), the heart (972), and renal proximal tubules (753 755). More important, however, is the ability of cells to adjust intracellular osmolarity by ion movement across the cell membrane and by generation, breakdown, uptake, or release of organic substances.

Ions contribute the bulk of intracellular (mainly K⁺) and extracellular (mainly NaCl) osmolarity. Furthermore, ions contribute some two-thirds to cell volume regulation after rapid alterations of extracellular osmolarity (331 1266). Thus ion transport across the cell membrane is of paramount importance for the regulation of cell volume. Largely because of volume regulatory ion transport, RVD and RVI are accomplished within minutes after exposure to anisotonic media.

A. Ions in Steady-State Maintenance of Cell Volume

To maintain their metabolic functions, cells have to accumulate a number of substances, such as proteins, amino acids, or carbohydrate metabolites. The concentration of these substances is higher within the cells than in extracellular fluid. The excess cellular concentrations of these organic substances are counterbalanced by lower intracellular ion concentration. Most cells extrude Na⁺ in exchange for K⁺ by the Na⁺-K⁺-ATPase. The cell membrane is only poorly permeable to Na⁺, and the exclusion of impermeable Na⁺ outweighs the cellular osmolarity created by impermeant organic solutes (double Donnan hypothesis; Refs. 721 776). On the other hand, the cell membrane is highly permeable to K⁺. The exit of K⁺ creates an outside-positive cell membrane potential, which drives Cl⁻ out of the cell. The low intracellular Cl⁻ concentration compensates for the excess intracellular concentration of organic substances.

Inhibition of the Na⁺-K⁺-ATPase with ouabain eventually leads to cell swelling (see Table 2) because of dissipation of the Na⁺ and K⁺ gradients, depolarization of the cell membrane, and subsequent entry of Cl⁻ into the cells (688 779). However, inhibition of the Na⁺-K⁺-ATPase does not always lead to a rapid increase of cell volume, which may remain constant (407 779 924 1039) or even transiently decrease (16 631 919 1131). A sequence of events leading to cell shrinkage after inhibition of the Na⁺-K⁺-ATPase includes increase of intracellular Na⁺ activity, reversal of Na⁺/Ca²⁺ exchange, increase of intracellular Ca²⁺ activity, subsequent activation of Ca²⁺-sensitive K⁺ channels, hyperpolarization (despite decrease of intracellular K⁺ activity), and cellular KCl loss. Obviously, the time required by ouabain to eventually cause cell swelling depends on Na⁺ entry. In thick ascending limb (519 520 1178) or diluting segment (444) of the nephron, for instance, swelling can be delayed by inhibition of Na⁺-K⁺-2Cl⁻ cotransport.

**Table 2. Factors altering cell volume**
Factor	Cell Affected
Factors leading to cell swelling

Insulin	Hepatocytes (4 472 473 953 1287 1286), pneumocytes (805)
IGF-I	Hepatocytes (1285)
Growth hormone	Chondrocytes (557)
ADH (AVP)	Glial cells (259 705)
Glucocorticoids	Hepatocytes (660)
	Fibroblasts (316)
Mineralocorticoids	Leukocytes (1329–1331)
Estrogens	Astrocytes (344)
	Parathyroid glands (137)
Progesterone	Astrocytes (344)
	Parathyroid glands (137)
Testosterone	Parathyroid glands (137)
Gonadotropin	Leydig cells (1346)
Somatostatin	Colon cells (277)
Adenosine	Erythrocytes (1132)
Angiotensin	Vascular smooth muscle cells (296)
Interleukin	Lymphocytes (1184)
α-Adrenergic	Hepatocytes (1286)
β-Adrenergic	Erythrocytes (56 323 459 862)
	Salivary glands (172)
	Sweat glands (907)
Acetylcholine*	Sweat glands (907)
	Myogenic L6 cells (1110)
Glutamate*	Glial cells (73 185 486–488 594 1084 1151)
	Neurons (185 186 975 1059)
Kainate	Neurons (24 999)
NMDA	Brain (190 1267)
Aspartate	Neurons (1059)
Deoxyadenosine	Lymphoblastoid cells (36)
cAMP	Sweat glands (907)
cGMP	Barnacle muscle (957)
PKC-ε,δ	Promyelocytes (1302)
Arachidonic acid	Glial cells (1147 1148)
ras Oncogene	Fibroblasts (695 824)
Phorbol esters	Necturus gallbladder (247)
Genistein	Tumor cells (925)
Okadaic acid	Erythrocytes (581 597 941)
Superoxide	Erythrocytes (1247)
Lithium	Erythrocytes (935 944)
Magnesium	Erythrocytes (332 943 944)
Amino acid uptake	Hepatocytes (43 51 60 204 342 471 502 653 654 1300 1341)
	Proximal renal tubule (67 69 122 173)
	Intestine cells (706 785 788 930 1092 1095)
Glucose uptake	Necturus gallbladder (355)
	Kidney (67)
	LLC-PK₁ cells (75)
	Intestine cells (785)
	Vascular smooth muscle cells (881)
	Mesangial cells (620)
Bile acids	Hepatocytes (497 506)
Increase of K⁺	Hepatocytes (1261)
	Gallbladder epithelium (229 528 639)
	Proximal renal tubule (261 631 689 1282)
	Renal cortical slices (973)
	Thick ascending limb (1178)
	Amphiuma diluting segment (443)
	Shark rectal gland (638)
	Glial cells (46 259 594 612 628 731 802 847 902 1086)
	Neurons (24 33 1086)
	Retinal Müller cells (312)
	GH-producing cells (307)
	Adrenal glomerulosa cells (513)
	Vestibular dark cells (1314)
Ba²⁺, quinidine*	Proximal renal tubule (1174 1282)
	Hepatocytes (12 498 618)
	A6 cells (272a)
	MDCK cells (1176)
Ouabain*	Necturus gallbladder (251 378)
	Thick ascending limb (1179)
	Collecting duct principal cells (1164 1165)
	Neurons (168)
	Platelets (806)
	Enterocytes (784)
	Sperm (258)
HCO⁻₃	Parotid glands (976)
Acidosis	Proximal renal tubule (1174 1175)
	Neurons (1149 1150)
	Glial cells (611 883 1145 1146 1149 1151 1172)
	Esophageal cells (1214)
(Short chain)fatty acids*	Enterocytes (278 280 1032)
	Proximal renal tubule (1016)
	Erythrocytes (385)
	Brain (178)
	Vestibular dark cells (1313)
	Shark rectal gland (315)
NH₃	Astrocytes (867 897 898)
	Opossum kidney cells (982)
Cytochalasin B	Lymphoblast cells (36)
Colchicine	Lymphoblast cells (36)
Vinblastine*	Lymphoblast cells (36)
Endotoxin	Hepatocytes (127)
N-methylformamide	HT-29 cells (260)
Chlorpromazine*	Erythrocytes (219 1205)
Hydroxyurea	Endothelial cells (2)
Ethanol	Hepatocytes (1362)
	Adenohypophysial cells (1063)
	Cardiac cells (552)
	Proximal tubule cells (600)
Dideoxycytidine	Monoblastoid cells (115)
Mercurials	MDCK cells (1028)
	Shark rectal gland (637)
Dioxin*	Hepatocytes (1344)
Veratridine	Neurons (190)
Hyperthermia	Chondrocytes (335)
	Osteoblasts (335)
Hemolysin	Erythrocytes (556)
Photofrin	Tumor cells (729 730)
Fertilization	Sperm (1212)
Electric field stimulus	Outer hair cells (906)
Factors leading to cell shrinkage

Glucagon	Hepatocytes (379 473 1287)
VIP	Intestine (276 901 1297)
Somatoliberin (hGHRH)	GH-producing cells (307)
ADH	MDCK cells (1176)
	Hepatocytes (1286)
Atriopeptin (ANF)	glial cells (705)
	Cardiac myocytes (198 199 201)
NO	Heart (200 201)
ATP	Endothelial cells (916)
	Hepatocytes (1286)
Bradykinin	Enterocytes (1210)
	Fibroblasts (1005)
	Ehrlich cells (547 1126)
	Endothelial cells (916)
Histamine	Enterocytes (1210)
	Ehrlich cells (547)
Thrombin	Enterocytes (1210)
	Ehrlich cells (547 1126)
Serotonin	Leech glial cells (46)
Adenosine	Renal collecting duct (1107)
	Hepatocytes (1286)
fMLP	Granulocytes (955)
Corticostatic peptides	Enterocytes (786)
α-Adrenergic	Hepatocytes (849)
	Salivary glands (797)
Isoprenaline	Nonpigmented ciliary epithelium (183)
Acetylcholine*	Salivary glands (338 341 699 797 846 872 873 882 911 976 1363)
	Sweat glands (1181 1189)
	Enterocytes (1210 1297)
PGE₂	Erythrocytes (743)
H₂O₂	Hepatocytes (470 1045)
cAMP	Necturus gallbladder (229 994)
	Hepatocytes (1286)
	MDCK cells (828 829 833 1176)
	Barnacle muscle (957 987)
	Pulmonary epithelium (787)
	Pancreatic epithelial cells (1182)
	Pancreatic epithelium (643)
	Intestine (1251)
	Nonpigmented ciliary epithelium (183)
cGMP	Heart (199 201)
A23187*	Pulmonary epithelium (787)
	Enterocytes (786 1210)
	Erythrocytes (134 310)
	Fibroblasts (1358)
	Neuroblastoma cells (233)
Thapsigargin	Enterocytes (786)
Okadaic acid*	Hepatocytes (101)
Cytochalasin B	MDCK cells (828 829)
Colchicine	Macrophages (821)
Ouabain	Neurons (16)
	Cardiac myocytes (1131)
	Vascular smooth muscle cells (919)
	Proximal renal tubules (631)
Decrease in K⁺_o	Erythrocytes (291)
	Leech glial cells (46)
	Pigmented ciliary epithelium (301)
Removal of Na⁺_o	Muscle cells (959)
	Pigmented ciliary epithelium (301)
Removal of Cl⁻_o	Kidney (777)
	Pigmented ciliary epithelium (301)
	Toad bladder (740)
	Amphibian skin (434 1246)
	Erythrocytes (933 939)
Removal of Ca²⁺_o	Muscle cells (958)
Mg²⁺ depletion	Erythrocytes (711)
Starvation	Hepatocytes (3 1140)
Heme oxygenation	Erythrocytes (163 164)
Elastin peptides	Tumor cells (946)
Urea	Proximal renal tubules (359)
	Hepatocytes (474)
	Erythrocytes (936)
Mastoparan	MDCK cells (1350)
NDS	Enterocytes (790)
Furosemide*	Macula densa cells (964)
	MDCK cells (1176)
MAG-3but	HL-60 leukemic cells (162)
Ethanol	Prolactin-secreting cells (1063 1068)
	Thyrotropin-releasing cells (1063)
Amphotericin B	Cornea epithelium (992)
	Macrophages (299)
Lead	Erythrocytes (310)
Cisplatin	Renal tubule cells (110)
Noise	Auditory hair cells (275)

VIP, vasoactive intestinal polypeptide; NDS, neutrophil-derived secretagogue; MAG-3but, monoacetone glucose 3-butyrate; NMDA, N-methyl-d-aspartate; IGF-I, insulin-like growth factor I; ADH, antidiuretic hormone; AVP, arginine vasopressin; PKC, protein kinase C; ANF, atrial natriuretic factor; NO, nitric oxide; PG, prostaglandin; fMLP, formyl-methionyl-leucyl-phenylalanine; hGHRH, human growth hormone-releasing hormone.

^{^*}Or similarly active drugs. Reference numbers are given in parentheses.

Under the influence of ouabain, hepatocytes and renal cortical cells are apparently able to maintain their cell volume by electrolyte accumulation in intracellular vesicles, which are subsequently expelled by exocytosis (1038 1039 1257–1260). The electrolyte accumulation is accomplished by a H⁺-ATPase in parallel to Cl⁻ channels (1039). At least theoretically, a H⁺-ATPase in the plasma membrane could similarly maintain cell volume by creating a cell negative potential difference across the cell membrane, thus driving Cl⁻ extrusion.

B. Volume Regulatory Ion Transport

As indicated above, ion transport across the cell membrane is the most efficient and rapid means of altering cellular osmolarity. During cell swelling, cells extrude ions, thus accomplishing RVD, whereas during cell shrinkage, cells accumulate ions to achieve RVI. The activation of ion release during RVD is paralleled by inhibition of ion uptake mechanisms, and the ion uptake during RVI is paralleled by inhibition of ion release mechanisms. Thus the simultaneous stimulation of ionic mechanisms for RVD and RVI is largely avoided (927 938). A tremendous amount of work has been dedicated to the elucidation of the ion transport systems in different tissues. A synopsis of tissue-specific transport systems is beyond the scope of this review and has been reviewed in detail elsewhere (682).

1. Regulatory cell volume decrease

The transport systems most often activated by cell swelling are separate K⁺ and anion channels. In several studies, the anion channels activated by cell swelling have been found to be nonselective, allowing the passage not only of Cl⁻ but also of HCO⁻₃ (690 1334) and even organic anions and neutral organic osmolytes (176 576 632 1034 1169).

Obviously, different channel proteins from different families are utilized for cell volume regulation. Among the cloned K⁺ channels invoked to serve cell volume regulation are the Kv1.3 (N-type K⁺ channel) (273), the Kv1.5 channel (316), and the minK channel (150 151). Cloned Cl⁻ channels invoked in cell volume regulation include the ClC-2 channel (435 584 585 760 1203), BRI-VDAC (272), I_Cln (158 439 440 910 948 949), and the P-glycoprotein (or MDR protein) (362 464 1015 1225 1249 1250). Alternatively, P-glycoprotein (490 532 589 590) and I_Cln (647) were suggested to regulate the volume regulatory Cl⁻ channel. However, the role of P-glycoprotein in cell volume regulation has been questioned (14 15 160 256 257 663 764 988 1217 1269). Clearly, many of the properties of cell volume regulatory anion channels are not explained by the known cloned channels (539), and additional anion channels must be operative. In addition, Na⁺(HCO⁻₃)_n cotransport may participate in RVD (1281). Apart from ion channels, the most frequently utilized transport system for KCl exit is electroneutral KCl cotransport (708–710 963 1206; for review, see Ref. 682). This transporter appears to be activated preferably by isotonic cell swelling (374). Some cells apparently release KCl by parallel activation of K⁺/H⁺ exchange and Cl⁻/HCO⁻₃ exchange (103 161). The H⁺ and HCO⁻₃ exchanged for KCl form CO₂ , which then diffuses out of the cell and is thus not osmotically active. Beyond that, the anion exchanger (AE1) has been implicated in activation of volume regulatory ion channels (374 861).

Swelling of Na⁺-rich erythrocytes is thought to stimulate Na⁺ extrusion through reversal of Na⁺/Ca²⁺ exchange, and parallel extrusion of Ca²⁺ by the Ca²⁺-ATPase (932). Alternatively, evidence has been presented for the activation of ouabain-insensitive Na⁺-ATPase or Na⁺-K⁺-ATPase (850). Swelling has been shown to stimulate (1263) or inhibit (1342) the Na⁺-K⁺-ATPase. The gastric K⁺-H⁺-ATPase is stimulated by cell swelling (1113).

In many cells, swelling leads to the activation of nonselective cation channels (for review, see Refs. 682 1040 1043). Because with the negative potential difference across the cell membrane the net driving force for cation movement is directed into the cell, ion movement through these channels cannot be expected to directly serve cell volume regulation. However, these channels allow the passage of Ca²⁺, which then enters the cells and activates Ca²⁺-sensitive K⁺ channels (187 1194 1234).

Usually more cations (K⁺ and Na⁺) are lost from cells than Cl⁻ (436 476 998). The difference is partially due to loss of HCO⁻₃. Most HCO⁻₃ lost is replaced by CO₂ , and the H⁺ thus generated is bound to intracellular buffers. Thus the exit of HCO⁻₃ is limited by the intracellular buffer capacity (346 738). The HCO⁻₃ that is replaced by CO₂ does not directly contribute to cell volume regulation but allows the cellular loss of K⁺.

Osmotic cell swelling decreases the gap junctional conductance (890 1002), an effect in part due to decrease of intracellular ion concentration.

Decreasing extracellular osmolarity activates Na⁺ channels in the frog skin (126 226), urinary bladder (329 740), and A6 cells (234), an effect, however, not related to cell volume regulation.

2. Regulatory cell volume increase

The major ion transport systems accomplishing electrolyte accumulation in shrunken cells are the Na⁺-K⁺-2Cl⁻ cotransporter (294 381) and the Na⁺/H⁺ exchanger (420). The latter alkalinizes the cell leading to parallel activation of the Cl⁻/HCO⁻₃ exchanger. The H⁺ and HCO⁻₃ exchanged for NaCl by the Na⁺/H⁺ exchanger and the Cl⁻/HCO⁻₃ exchanger are replenished within the cell from CO₂ , which diffuses into the cell and is thus osmotically not relevant.

Among the cloned members of the Na⁺/H⁺ exchanger family (1294), NHE-1 (266), NHE-2 (266 601), and NHE-4 (107) are stimulated, whereas NHE-3 (86 87 266 601) is inhibited by cell shrinkage. The putative volume-sensitive site at the NHE-1 molecule has been identified and is distinct from the sites regulated by Ca²⁺ and growth factors (86). The cloned anion exchanger AE2 but not AE1 is postulated to participate in RVI (587).

Several members of the volume regulatory Na⁺-K⁺-2Cl⁻ cotransporters have been cloned (265 364 951 952 1370). In muscle cells, NaCl cotransport rather than Na⁺-K⁺-2Cl⁻ cotransport is utilized for NaCl uptake (288). However, little is known about the volume regulatory role of the cloned NaCl cotransporters (365).

In some cells, electrolyte accumulation during RVI is accomplished by activation of Na⁺ channels and/or nonselective cation channels (159 177 1278 1332). The depolarization induced by the Na⁺ entry favors Cl⁻ entry into the cell.

On the other hand, cell shrinkage has been shown to inhibit K⁺ and Cl⁻ channels, preventing cellular electrolyte loss through those channels (for review, see Ref. 682). In several cell types, shrinkage has been observed to activate the Na⁺-K⁺-ATPase, which serves to replace accumulated Na⁺ with K⁺ (for review, see Ref. 682).

Some cells do not undergo RVI during exposure to hypertonic extracellular fluid. The same cells, if exposed to hypotonic extracellular fluid, show RVD, and if reexposed to isotonic fluid, first shrink and then display RVI (secondary RVI or RVI on RVD). In these cells, primary RVI is presumably prevented by increased intracellular Cl⁻ activity, as detailed in section iiiI.

C. Osmolytes

The cellular accumulation of electrolytes after cell shrinkage is limited because high ion concentrations interfere with structure and function of macromolecules, including proteins (25 139 192 193 413 491 564 573 1376 1381). Furthermore, alterations of ion gradients across the cell membrane would affect the respective transporters. An increase of intracellular Na⁺ activity, for instance, would reverse Na⁺/Ca²⁺ exchange and thus increase intracellular Ca²⁺ activity, which would in turn affect a multitude of cellular functions (1226).

To circumvent the untoward effects of disturbed ion composition, cells produce so-called osmolytes, molecules specifically designed to create osmolarity without compromising other cell functions (37 44 141 371 384 484 629 630 714 875 1138 1377 1378). Unlike ions, organic osmolytes even at high concentrations are compatible with normal macromolecular function. Thus the term compatible osmolytes has been coined (129).

Three groups of osmolytes are used in mammalian cells: polyalcohols, such as sorbitol and inositol; methylamines, such as glycerophosphorylcholine and betaine; and amino acids and amino acid derivatives, such as glycine, glutamine, glutamate, aspartate, and taurine (141 368 370 371 629 630 714 719 724 1077 1381). Tissue-specific utilization of the various osmolytes has been reviewed elsewhere in detail (682).

Osmolytes are specifically important for cell volume regulation in renal medulla, where extracellular osmolarity may become more than fourfold that of isotonicity (62 64–66 99 112 141 369 399 442 452 525 666 718 724 855 1075 1076 1078 1352 1353 1356 1377 1378), and in the brain, where cell volume alterations cannot be tolerated due to the rigid skull and where alterations of ion composition would affect excitability (453 524 715–717 745 746 915 1155 1166 1167 1170 1220 1221 1266 1270).

Osmolytes not only replace ions as osmotically active species but also stabilize macromolecules, thus counteracting the adverse effects of inorganic (such as K⁺, Na⁺, and Cl⁻) and organic (such as spermine) ions (26 138 139 213 334 662 1271 1351). Furthermore, betaine and glycerophosphorylcholine, and to a lesser extent inositol, counteract the destabilizing effect of urea on proteins (145 203 384 483 750 879 966 1119 1380 1382). For normal cell function, an appropriate balance must be maintained between destabilizing (i.e., ions, urea) and stabilizing (i.e., counteracting osmolytes) forces (19 267 807 863 1272 1376 1383). Accordingly, an increase of urea concentration specifically favors the parallel increase of glycerophosphorylcholine (723 855 966).

Beyond their function in cell volume regulation, osmolytes are protective against the destructive effects of excessive temperatures (34 292 352 383 534 579 759 926 989 1058 1160 1193 1200) and dessication (169 232). Furthermore, they have been found to ease cell membrane assembly (642).

Cellular osmolyte accumulation can be achieved by stimulated uptake, enhanced formation, or decreased degradation. Decrease of intracellular osmolyte concentration is accomplished by degradation or release. As compared with RVI accomplished by ions, accumulation of osmolytes is a slow process taking hours to days.

1. Glycerophosphorylcholine

Glycerophosphorylcholine (GPC) is formed by deacylation of phosphatidylcholine. The reaction is catalyzed by a phospholipase A₂ , which is distinct from the arachidonyl-selective enzyme (370 371). Glycerophosphorylcholine is broken down by the GPC phosphodiesterase, which degrades GPC to glycerol phosphate and choline (370 371). Increase of osmolarity by extracellular addition of either NaCl or urea inhibits the phosphodiesterase and thus leads to accumulation of GPC (1243).

2. Sorbitol

Sorbitol is produced from glucose under the catalytic influence of aldose reductase (70 321 373), an enzyme that is distributed in various tissues (104 140 217 358 614 765 856 1053–1055 1102 1198). The enzyme is upregulated by hypertonic extracellular addition of NaCl or raffinose, but not of membrane-permeable solutes, such as urea or glycerol. It is presumably an increase of cellular ionic strength that stimulates the aldose reductase transcription rate (40 230 373 599 854 1130 1236). With continued hyperosmotic stress, the enzyme activity and thus sorbitol concentration increases slowly, approaching maximal values within 3 days (372). Osmolarity does not affect mRNA stability or enzyme degradation (39 854). The half-life of the enzyme is ∼6 days (372). Cell swelling stimulates the release of sorbitol (39 377 1345) through putative channels, which are thought to be inserted into the cell membrane by fusion of vesicles (629).

3. Inositol

Myo-inositol (inositol) is taken up into cells by a Na⁺-coupled transporter (81 480 666–668 670 1375). Increased cellular ionic strength (141) but not urea (878) stimulates the transcription of the transporter and thus cellular inositol accumulation (877 1372). Similar to sorbitol, inositol is rapidly released from swollen cells (354 630).

4. Betaine

Betaine is accumulated in cells by a Na⁺-coupled transporter (149 1190 1372 1374). The carrier prefers γ-aminobutyric acid (GABA), which, however, is minimally available in extracellular fluid (1374). Increased cellular ionic strength (1242), but not urea (878), stimulates the transcription rate of the transporter and thus betaine accumulation (876 878 1191 1372). Betaine may further be accumulated by choline oxidation, which is, however, sensitive to cell shrinkage only in renal cortex (433 758). After cell swelling, betaine is rapidly released (354 630).

5. Taurine

Taurine is accumulated in cells by a Na⁺-coupled transporter (1239). The transcription of the transporter is stimulated by enhanced ionic strength, eventually leading to cellular taurine accumulation (1238 1240). After cell swelling, taurine is rapidly released, presumably through an anion channel (102 540 632 671 672 678 847 1050 1087 1238 1240) which is, at least in Ehrlich ascites tumor cells, distinct from the volume regulatory Cl⁻ channel (677). In oocytes, expression of band 3-anion exchanger tAE1 confers volume regulatory taurine transport (324 374 861), but in mammalian cells, taurine efflux is not dependent on the presence of band 3 protein (1049). On the other hand, taurine transport is induced by the insertion of the peptide phospholemman (PLM) in lipid bilayers (845).

6. Amino acids

In addition to taurine, the cellular concentration of several other amino acids and amino acid metabolites is modified by cell volume, including glutamine, glutamate, glycine, proline, serine, threonine, β-alanine, (N-acetyl)aspartate, and GABA (for review, see Refs. 181 682). Although the intracellular concentration of most individual amino acids is quite low, the sum of all amino acids significantly contributes to cellular osmolarity in cells exposed to isotonic extracellular fluid (714). Cell shrinkage stimulates Na⁺-coupled transport of neutral amino acids (182 380 1135 1373) and proteolysis (498) and inhibits protein synthesis (1159). Conversely, cell swelling inhibits proteolysis and stimulates protein synthesis (498 499 1159). Furthermore, cell swelling stimulates breakdown of glutamine and glycine (496 500) as well as cellular release of several amino acids (540), at least partially through volume regulatory anion channels (176). Accordingly, cellular amino acid concentration increases upon cell shrinkage and decreases upon cell swelling (714). In fibroblasts, the major amino acid accumulated is glutamine (238 239). Amino acids are probably important during adaptation to minor changes of extracellular osmolarity. Their contribution is, however, negligible for the adaptation to the excessive osmolarities in kidney medulla (714).

D. Further Metabolic Pathways Contributing to Cell Volume Regulation

In addition to amino acids, numerous organic metabolites contribute to cellular osmolarity. Several metabolic pathways known to be sensitive to cell volume may modify the concentrations of these metabolites and thus contribute to cell volume regulation. Cell swelling increases glycogen synthesis and inhibits glycolysis, thus decreasing the concentration of carbohydrate metabolites (12 49 50 696 819 953). Furthermore, cell swelling has a relatively weak stimulatory effect on lipogenesis (51). As detailed in section vC, cell volume changes interfere with a great number of other metabolic functions that to some extent may modify cellular osmolarity. The overall impact of these effects on cellular osmolarity is probably modest, but the influence of cell volume on various metabolic pathways is of paramount importance for regulation of metabolic function (see sect. vC).

III. INTRACELLULAR SIGNALING OF CELL VOLUME REGULATION

Cell swelling and shrinkage exert profound effects on intracellular signaling mechanisms, which in turn modify a multitude of cellular functions including the volume regulatory mechanisms. A great deal of experimental effort has been spent in elucidating the intracellular machinery underlying cell volume regulation. Frequently, the result has been inconclusive for several reasons. 1) Not every effect of altered cell volume on intracellular signaling is related to regulation of cell volume. 2) Cells usually use several mechanisms in parallel, with different, partially overlapping cellular signaling mechanisms. 3) Different cells utilize distinct mechanisms, i.e., the information gained in any given cell cannot necessarily be generalized to other cells. 4) Volume regulation requires mechanisms that are themselves not modified by cell volume changes but rather permissive for activation of cell volume regulatory mechanisms.

In the simplest case, an intracellular mechanism serves cell volume regulation if it is modified by alterations of cell volume, and a qualitatively and quantitatively identical modification of this intracellular mechanism triggers the appropriate alterations of cell volume. This requirement frequently is not met. If the identical modification does not trigger respective alterations of cell volume, the participation of a mechanism in cell volume regulation still cannot be ruled out, since the mechanism may require the collaboration of other mechanisms to be effective. Similarly, the use of inhibitors, even if they are specific, does not lead to conclusive results. On the one hand, inhibition of cell volume regulation by elimination of a given element of intracellular signaling (e.g., inhibition of protein kinases or removal of Ca²⁺) does not discriminate between volume regulatory and permissive mechanisms. On the other hand, cell volume regulation may prove insensitive to elimination of a volume regulatory mechanism if other mechanisms operating in parallel are strong enough to replace the defect. Further examples could be given, each of which illustrates that the experimental elucidation of the complex machinery serving cell volume regulation is extremely difficult.

Even though our understanding of the intracellular machinery mediating cell volume regulation is still incomplete, knowledge of the interaction between cell volume, elements of cellular signaling, and cell volume regulatory mechanisms is mandatory for understanding the role of cell volume for cell function.

A. Macromolecular Crowding

Cell swelling leads to dilution and cell shrinkage to concentration of cellular constituents including proteins. The concentration of intracellular proteins markedly influences their function (131 353 376 834 836 937 1011). In erythrocytes, the volume regulatory set point can indeed be varied by manipulation of intracellular protein concentration (835 837 1397). The set points of both the KCl symport (835 838) and the Na⁺/H⁺ exchanger (209 210 940) appear to be determined by macromolecular crowding. It has been suggested that among the enzymes sensitive to ambient protein concentration is a kinase that is inactivated by protein dilution during cell swelling and activated by protein crowding during cell shrinkage (835 838). This kinase may inhibit the volume regulatory KCl cotransport. Its inactivation during cell swelling would then disinhibit volume regulatory KCl efflux.

Because of interaction of proteins with ambient electrolytes, macromolecular crowding is reduced by increasing ionic strength, which indeed shifts the volume regulatory set point to smaller volumes (942).

Similarly, urea decreases the thermodynamic activity of proteins and thus reduces macromolecular crowding (211 574 723 837 978 984 1376). Urea has been shown to activate erythrocyte KCl transport (293 596 936), erythrocyte Na⁺/Ca²⁺ exchange (936), and hepatocyte K⁺ channels (474) and to inhibit Na⁺/H⁺ exchanger in erythrocytes (936) and adenosine 3′,5′-cyclic monophosphate (cAMP) production (58), Na⁺/H⁺ exchanger (732), and Na⁺-K⁺-2Cl⁻ cotransport (595) in thick ascending limb cells, thus leading to cell shrinkage. In erythrocytes, the effect of urea was reversed by okadaic acid, pointing to the involvement of phosphorylation (936).

B. Cytoskeleton

1. Actin filaments

Obviously, cell swelling or shrinkage will affect the cytoskeletal architecture. In fact, actin filaments have been found to be depolymerized during swelling of a variety of cells (89 220–223 241 477 478 527 736 830 831 848 1209 1398), an effect which is at least partially due to Ca²⁺ (223). Calcium concentration increases in most cells after osmotic swelling (see sect. iiiF ). As a result, Ca²⁺ depolymerizes actin filaments by binding to gelsolin (1161 1327). Depolymerization could further result from degradation of phosphatidylinositol 4,5-bisphosphate, which inhibits depolymerization by interaction with profilin (703 704). A transient depolymerization of the actin filaments may be followed by a polymerization of actin filaments (1398). In hepatocytes, polymerization of actin filaments prevails (1202) and is paralleled by expression of β-actin (1097 1202). The de novo actin biosynthesis is probably the result of actin polymerization, since it is inhibited by depolymerized actin (993).

Cytoskeletal elements may interfere in several ways with volume regulatory mechanisms. Actin filaments may inhibit osmotically driven water fluxes (566 567) and thus retard osmotically induced cell volume changes. Beyond that, RVD is inhibited in several tissues by cytochalasin D (89 221 222 224 289 340 363 619 754 1258), which interferes with actin assembly (781 1161). Moreover, expression of actin binding protein was required for RVD in melanoma cells (166). Thus an intact actin filament network is required for activation of at least some of the volume regulatory mechanisms. In fibroblasts, actin depolymerization reverses the shrinking effect of bradykinin into a swelling effect, again pointing to a role of actin filaments in cell volume control (1001 1004). Via other cytoskeletal elements, such as spectrin and ankyrin, actin filaments couple to membrane proteins, an interaction modified by cell volume changes. For instance, cell swelling stimulates binding of ankyrin to the anion exchanger band 3 protein (868). Another putative target of the actin filament network is a K⁺ channel that cannot be activated in isolated membrane vesicles devoid of cytoskeleton (423). Furthermore, it has been shown that actin filament fragments regulate Na⁺ channels (77), and it has been speculated that the cytoskeleton may participate in the insertion of cell volume regulatory channels into the plasma membrane (340 741), in the regulation of channels by kinases (see sect. iiiH) and phospholipids (see sect. iiiK), and in the activation of channels by membrane stretch (1040). However, disruption of the actin network did not prevent activation of channels by cell membrane stretch (1133). Furthermore, the stimulation of taurine or inositol release during cell swelling was not affected by cytochalasin B (626 848).

The depolymerization of the actin filament network may participate in the activation of a mechanosensitive anion channel (832 1108 1227). Furthermore, depolymerization of submembranous actin filaments may facilitate the fusion of channel-containing vesicle membranes with the plasma membrane. Agonist-induced exocytosis has indeed been shown to be favored by actin depolymerization (32 130 147 283 954).

The cytoskeleton is further thought to be involved in the volume regulatory activation of the Na⁺/H⁺ exchanger (106 404 431 1292), which does contain putative cytoskeletal binding sites (333). Actin depolymerization by either cell swelling or by addition of cytochalasin B, however, activates the Na⁺-K⁺-2Cl⁻ cotransporter (541 586 813), and in vesicles devoid of cytoskeleton, the Na⁺-K⁺-2Cl⁻ cotransporter is permanently active (541). This activation is counterproductive during the initial phase of cell swelling.

In addition to its role in regulation of ion transport, the cytoskeleton may mediate some effects of cell volume on gene expression (76 529).

2. Microtubules

Cell swelling increases microtubule stability and stimulates the expression of tubulin (511).

Colchicine, which disrupts the microtubule network, inhibits RVD in Jurkat cells, HL-60 cells, and peripheral neutrophils (289), but not in Ehrlich ascites tumor cells (223), kidney cells (924), and gallbladder (340). In macrophages, disruption of microtubules was found to activate anion channels (821).

An intact microtubule network was found to be crucial for the influence of cell volume on alkalinization of intracellular vesicles (156 1089), proteolysis (156 1284), and taurocholate exit from liver cells (508).

C. Cell Membrane Stretch

A variety of ion channels are activated by cell membrane stretch, i.e., increased tension of the cell membrane (1040 1043). Stretch increases the open probability of the channels without affecting single-channel conductance or selectivity of the channels (1043).

The stretch-activated channels may be selective for K⁺ or for anions, thus directly serving cell volume regulation (857 1043). Most of these channels, however, are nonselective cation channels, allowing the passage of K⁺, Na⁺, and Ca²⁺ (for review, see Refs. 682 1043). Because of the cell-negative cell membrane potential, the respective electrochemical gradients favor the cellular accumulation of Na⁺ and Ca²⁺ rather than cellular loss of K⁺. Thus these channels are not likely to directly serve cell volume regulation, and inhibition of these channels by gadolinium has been shown to decrease osmotic swelling and favor regulatory decrease of cell volume (1173). On the other hand, Ca²⁺ entering the cells through these channels is thought to activate Ca²⁺-sensitive K⁺ channels (187 1194 1234).

The mechanism linking membrane stretch to activation of the channels has not been clearly defined (1043). Under discussion are 1) release of fatty acids from the stretched membrane and subsequent activation of stretch-sensitive channels by these fatty acids (917) and 2) stretch-induced activation of some element of the cytoskeleton, such as spectrin (1133). Because stretch enhances channel open probability in the cell-free excised patch configuration (1043), cytosolic components are apparently not required for channel activation.

It is debatable whether stretch-activated channels participate in the fine-tuning of cell volume, since considerable stretch is required to activate these channels (1043). Possibly, these channels may represent a last line of defense against excessive cell swelling but are not involved in the response to moderate changes of cell volume.

D. Cell Membrane Potential

The influence of cell swelling on cell membrane potential depends on the ion channels preferentially activated or inactivated and on the potential difference before cell swelling. Activation of K⁺ channels and a low initial cell membrane potential favor hyperpolarization, whereas activation of anion or nonselective cation channels and a high initial cell membrane potential would favor depolarization. After cell swelling, hyperpolarization of the cell membrane is seen in hepatocytes (406), depolarization of the cell membrane in Ehrlich ascites tumor cells (680 691), Madin-Darby canine kidney (MDCK) cells (947), opossum kidney cells (1235), lymphocytes (418 419 1060), pancreatic β-cells (124), astrocytes (627), neuroblastoma cells (313), and vascular smooth muscle cells (685). In some cells, a transient hyperpolarization due to activation of K⁺ channels is followed by a more sustained depolarization due to activation of anion channels (516–518 1002).

The alteration of cell membrane potential may influence the activity of additional ion channels. A depolarization of the cell membrane may open voltage-sensitive ion channels. In lymphocytes, RVD involves n-type K⁺ channels (273 429), which are activated by cell membrane depolarization. Depolarization of the cell membrane may further activate voltage-sensitive Ca²⁺ channels, as observed in pancreatic β-cells (124) and vascular smooth muscle cells (685). The increase of intracellular Ca²⁺ could trigger a variety of further mechanisms, as illustrated in section v, E and F.

As discussed in section iiB, increase of extracellular osmolarity may either depolarize or hyperpolarize cells due to activation of unspecific cation channels or inhibition of K⁺ and/or Cl⁻ channels.

E. Cytosolic pH

Cell swelling leads to cytosolic acidification (216 397 479 610 616 685 757 864 1002 1089 1143 1279), which has been explained by the exit of HCO⁻₃ through anion channels (1334), by release of H⁺ from acidic intracellular compartments (see sect. iiiL), and by enhancement of Cl⁻/HCO⁻₃ exchange due to decreasing cellular Cl⁻ activity (757). This latter mechanism, however, should be impeded by inhibition of the exchanger at acidic cytosolic pH (645), and cellular acidosis is not inhibited by removal of extracellular Cl⁻, at least in osteosarcoma cells (864).

Cell shrinkage is frequently observed to alkalinize cells, at least partially due to activation of volume regulatory Na⁺/H⁺ exchange (see sect. iiB).

The impact of intracellular pH on volume regulatory mechanisms has not been explored. After cell swelling, the cytosolic acidification may impede activation of volume regulatory K⁺ channels (783) and may contribute to inhibition of glycolysis and thus to the decreased release of lactic acid (696). The alkalinization after cell shrinkage should stimulate glycolysis (696).

F. Calcium

After cell swelling, intracellular Ca²⁺ concentration ([Ca²⁺]_i) increases in a variety of cells, whereas it remains apparently constant in others (for review, see Refs. 682 815). Swelling may increase [Ca²⁺]_i by both activation of Ca²⁺-permeable channels in the cell membrane and Ca²⁺ release from intracellular stores. Calcium-permeable channels may be activated by cell membrane stretch (see sect. iiiC ), cell membrane depolarization (see sect. iiiD), and/or protein kinase C (1066). Calcium release from intracellular stores is presumably triggered by inositol phosphates (52 72 1180 1288 1289) or Ca²⁺-induced Ca²⁺ release (516 518). The regulation of [Ca²⁺]_i by cell volume may interfere with signaling of Ca²⁺-recruiting hormones, as shown for gastric parietal cells (885) and HT-29 cells (330). In those cells, agonist-induced entry of Ca²⁺ was further stimulated by cell swelling (330 885) and inhibited by cell shrinkage (885).

The increase of [Ca²⁺]_i accounts for the activation of Ca²⁺-sensitive K⁺ channels, as shown in Ehrlich ascites tumor cells (188), MDCK cells (1334), proximal tubule cells (290 605), thick ascending limb cells (1194), choroid plexus epithelial cells (187), and neuroblastoma cells (313). In MDCK cells, [Ca²⁺]_i did not appreciably increase upon moderate osmotic cell swelling, even though the Ca²⁺-sensitive K⁺ channels were already activated by this treatment (1002). Possibly small, localized increases of [Ca²⁺]_i are sufficient to activate the K⁺ channels but are not detected by fluorescence measurements (1357).

Despite the activation of Ca²⁺-sensitive K⁺ channels, RVD is apparently not mediated by a rise of [Ca²⁺]_i in Ehrlich ascites tumor cells (1204), and swelling-induced K⁺ efflux was virtually unaffected by the inhibitors of the Ca²⁺-sensitive K⁺ channels, clotrimazole and charybdotoxin (489). Because these K⁺ channels are inwardly rectifying (1334), K⁺ exit through these channels during cell swelling may be limited by the depolarization of the cell membrane. Other less inwardly rectifying K⁺ channels may thus be more important for cell volume regulation in those cells (539). In a variety of tissues, increase of [Ca²⁺]_i was not required for RVD (for review, see Ref. 682). Clearly, activation of K⁺ channels by Ca²⁺ may contribute to, but is frequently not crucial for, RVD (539).

In contrast to volume regulatory K⁺ channels in many tissues, volume regulatory Cl⁻ channels have been found to be insensitive to Ca²⁺ in intestinal cells (517 657), ciliary epithelial cells (1385), cardiac myocytes (1227), T84 colon carcinoma cells (1134 1364), airway epithelial cells (361 1134), MDCK cells (48 1029 1334), lymphocytes (421), Ehrlich cells (188), and chromaffin cells (287). Yet, as shown in Ehrlich ascites tumor cells, Ca²⁺ triggers the formation of leukotrienes, which do activate the channels (539). In kidney cortex, Ca²⁺-sensitive Cl⁻ channels have been found in endosomes and proposed to serve cell volume regulation (991). Calcium is also thought to trigger the fusion of vesicles, allowing the release of sorbitol (629), whereas it is apparently not required for release of GPC (629) or taurine (1051).

Calmodulin antagonists and inhibitory peptides against Ca²⁺/calmodulin-dependent kinase (116) have been shown to inhibit RVD or activation of cell volume regulatory ion channels (71 263 421 424 543 546 815), and it has been concluded that calmodulin/Ca²⁺ complexes are important for activation of RVD. In other cells, however, Ca²⁺-sensitive K⁺ channels involved in cell volume regulation did not require calmodulin and were actually activated by calmodulin antagonists (950).

Beyond its putative role during RVD, calmodulin has been implicated in activation of the Na⁺-K⁺-2Cl⁻ cotransport in RVI (583).

G. G Proteins

Inhibitors of G proteins such as pertussis toxin or cholera toxin have been shown to blunt the RVD (539) as well as swelling-induced osmolyte efflux (1037), increases of intracellular Ca²⁺ concentration (30), mitogen-activated protein kinase (MAPK) activity (895 1072), vesicular acidification (1088), and swelling-induced stimulation of taurocholate excretion (895), suggesting that G proteins do mediate some effects of cell swelling. Activation of the Na⁺/H⁺ exchanger during cell shrinkage has similarly been claimed to involve G proteins (108 249).

In addition to heterotrimeric G proteins, small G proteins have been implicated in cell volume regulation. Clostridium botulinus C₃ exoenzyme, which depolymerizes the actin filament network by ADP-ribosylation of rho (8), blunts the volume regulatory anion efflux (1209). In neurons, osmotic cell shrinkage stimulates the expression of α₁-chimerin (286), a GTPase-activating protein that inactivates the small G protein Rac. The impact of this effect on cell volume regulation is not explored.

H. Protein Phosphorylation

1. Cell swelling

Mechanical stress or cell swelling has been found to stimulate protein kinase C (997 1017) to foster tyrosine phosphorylation of several proteins including focal adhesion kinase p125^FAK (1209 1211), to stimulate phosphatidylinositol 3-kinase (PI 3-kinase) (1209), and to trigger MAPK cascades leading to the activation of Jun-NH₂-terminal kinase (JNK) or extracellular signal-regulated kinases ERK-1 and ERK-2 (4 360 482 568 569 895 1044 1072 1073 1127 1211). Adenylate cyclase has been reported to be stimulated (851 1324–1326) and inhibited (535) by cell swelling, and cAMP has been shown to inhibit volume regulatory Cl⁻ channels in chicken hearts (468). Most recently, we have successfully cloned a cell volume-regulated serine/threonine kinase, the human serum glucocorticoid-dependent kinase h-sgk (1295). Expression of this kinase is rapidly upregulated by moderate cell shrinkage and markedly depressed by moderate cell swelling.

How these events link to activation of the various volume regulatory mechanisms is poorly understood. The volume regulatory KCl cotransport is activated by dephosphorylation and inactivated by phosphorylation (94 295 580 581 597 920 1144). Swelling or increased hydrostatic pressure was suggested to inhibit a kinase, favoring dephosphorylation (94 295 386 580), but nothing is known about the properties of this kinase, which appears to be distinct from protein kinases A and C (581). Some evidence indicates the involvement of the cytoskeleton in the swelling-induced inhibition of the kinase (539). On the other hand, the view that phosphorylation or dephosphorylation links cell swelling to activation of KCl cotransport has been challenged (1041).

The volume of a wide variety of cells is decreased by cAMP (see Table 2), an effect mainly due to activation of Cl⁻ channels and K⁺ channels. To the extent that in those cells cAMP is increased after cell swelling, cAMP participates in cell volume regulation. Beyond that, cAMP has been postulated to shift the volume regulatory set point of the channel toward smaller volumes (823).

Additional experimental evidence points to the involvement of various kinases in volume regulation of different cell types. In intestinal cells, volume regulatory rubidium efflux was inhibited by herbimycin A and genistein, pointing to involvement of tyrosine kinase (1211). Swelling of Jurkat cells activates the src-like tyrosine kinase p56^lck, which in turn accounts for the activation of the volume regulatory Cl⁻ channels (727a). Wortmannin, an inhibitor of PI 3-kinase, similarly interferes with cell volume regulation in those cells (1209). In proximal tubules (1012–1014) and in HeLa cells (490), protein kinase C has been invoked to link cell swelling to activation of Cl⁻ channels. Cell swelling leads to phosphorylation of the anion exchanger, which was postulated to release taurine (869).

In addition to its role in the phosphorylation of proteins, ATP may serve as a signaling molecule itself. The volume regulatory Cl⁻ channel in collecting duct, glioma, and intestine 470 cells (908 1277) as well as taurine efflux in skate hepatocytes and glioma cells (47 575 1277) are apparently regulated by intracellular ATP concentration. Decreased ATP concentration, as it occurs during energy depletion, inhibited the channel. In pancreatic β-cells, cell swelling leads to activation of ATP-sensitive K⁺ channels (289a). Extracellular ATP has been shown to stimulate taurine release from tracheal cells (362). It has been speculated that after cell swelling ATP is extruded via the cystic fibrosis transmembrane conductance regulator and activates K⁺ channels and Cl⁻ channels from the extracellular side (1030 1310). On the other hand, extracellular ATP has been shown to inhibit volume regulatory Cl⁻ channels in intestinal cells (1228).

2. Cell shrinkage

Similar to cell swelling, osmotic cell shrinkage has been shown to activate protein kinase C (702), whereas cAMP formation (648) and cAMP-dependent phosphorylation have been shown to remain unaffected (13 648). In several cell types, osmotic shrinkage stimulates the phosphorylation of myosin light chains, an effect presumably related to activation of Na⁺-K⁺-2Cl⁻ cotransport (635 903 1188).

Excessive osmotic cell shrinkage, such as doubling of extracellular osmolarity, triggers several proteins involved in the MAPK pathways, such as Raf-1, MAPK kinase, MAPK, and ribosomal protein S6 kinase (809 1197) or activation of JNK by the MAPK kinase MKK4 (853), which may be triggered by the tyrosine kinase Pyk2 through a pathway requiring activation of PI 3-kinase and the small G proteins Ras and Rac (1216). The activation of MAPK pathways may be secondary to clustering and internalization of cytokine receptors with subsequent activation of downstream targets (1020). On the other hand, the ribosomal protein S6 has been reported to be dephosphorylated upon osmotic cell shrinkage (656).

As shown in several tissues, cell shrinkage stimulates serine and threonine phosphorylation of the Na⁺-K⁺-2Cl⁻ cotransporter (636 772 927 968 1219). Volume-regulated Na⁺-K⁺-2Cl⁻ cotransport may be activated (812 814 968) or inhibited (728) by cAMP, and cAMP does not participate in activation of this carrier during cell shrinkage (381). The protein kinase C inhibitor chelerythrine (702), but not staurosporine (583 919), inhibits volume regulatory Na⁺-K⁺-2Cl⁻ cotransport, which may be activated (583) or inhibited (728) by phorbol esters. The involvement of protein kinase C in the activation of this carrier is thus a matter of debate.

Even though the Na⁺/H⁺ exchanger is activated by phosphorylation (88), phosphorylation of the carrier is not affected by cell shrinkage (430) and not required for activation (430). In Ehrlich ascites tumor cells, shrinkage-induced activation of the transporter has been reported to be blunted by inhibition of protein kinase C and stimulated by inhibition of phosphatases (956). In dog erythrocytes, inhibition of phosphatases shifted the set point of the Na⁺/H⁺ exchanger to higher volumes (941). However, protein kinase C appeared not to be involved in activation of the carrier in other tissues (108 244 422 426 427).

The role of MAPKs in triggering of cell volume regulatory mechanisms remains elusive, whereas their involvement in regulation of betaine transporter expression has been ruled out (669).

In yeast, histidine kinases are activated by enhanced osmolarity and trigger a cascade involving a MAPK-like protein (791). Up to now, attempts to identify a volume-regulated histidine kinase in mammalian cells have failed.

I. Chloride

As pointed out in section iiA, intracellular Cl⁻ activity is kept low, and this counterbalances the high intracellular osmolarity created by organic substances. During osmotic cell swelling, intracellular Cl⁻ activity is expected to decrease further due to H₂O entry during the swelling phase and Cl⁻ release during RVD. Intracellular Cl⁻ activity is similarly expected to decrease during swelling by cumulative substrate uptake, but it should increase during swelling by depolarization of the cell membrane or after stimulation of Na⁺-K⁺-2Cl⁻ cotransport.

Osmotic cell shrinkage is expected to increase intracellular Cl⁻ activity due to cellular H₂O loss during the shrinking phase and Cl⁻ accumulation during RVI. On the other hand, intracellular Cl⁻ activity should decrease during shrinkage caused by activation of ion channels.

Decreased intracellular Cl⁻ activity is apparently required for full activation of Na⁺-K⁺-2Cl⁻ cotransport during cell shrinkage (539 548 1245 1370). Beyond its influence on one of the driving forces of Na⁺-K⁺-2Cl⁻ cotransport, a decreased intracellular Cl⁻ concentration is thought to play a permissive role for the activation of both Na⁺-K⁺-2Cl⁻ cotransport (119 734 735 1009) and Na⁺/H⁺ exchange (108 250 933 934 1009). If extracellular osmolarity is made hypertonic by increased extracellular NaCl concentration, the increase of intracellular Cl⁻ activity could thus impede RVI (539). Accordingly, some cells are unable to regulate their volume during exposure to hypertonic extracellular fluid (308 437 522 539 544 545 634). If intracellular Cl⁻ is lowered by prior RVD (308 420 522 634) or by activation of Cl⁻ channels with cAMP (437 1177) or vasopressin (351 519 1177), the same cells do accomplish RVI. Moreover, if cells are exposed to short-chain fatty acids, they swell by accumulation of the acids along with Na⁺ and are forced to release Cl⁻ for RVD (see Table 2). In the presence of these acids, they display RVI after exposure to hypertonic extracellular fluid (1016).

Intracellular Cl⁻ inhibits the glycogen synthase phosphatase (408), and the decrease of intracellular Cl⁻ activity participates in the stimulation of glycogen synthesis during osmotic or glutamine-induced cell swelling (555 819).

J. Magnesium

The dilution and concentration of intracellular solutes during cell swelling or shrinkage lead to the respective alterations of Mg²⁺ concentration. Magnesium has been described to inhibit volume regulatory KCl cotransport (78 295). During cell swelling, the decrease of intracellular Mg²⁺ concentration may partially account for the activation of KCl cotransport (78 295). Conversely, an increase of intracellular Mg²⁺ activity stimulates Na⁺/H⁺ exchange (944) and Na⁺-K⁺-2Cl⁻ cotransport (794) and may thus participate in regulatory cell volume increase.

K. Eicosanoids

Cell swelling has been shown to activate phospholipase A₂ (542 800), possibly in part through decrease of macromolecular crowding (539). Metabolites of arachidonic acid include the products of cyclooxygenase (e.g., prostaglandins), 15-lipoxygenase (such as hepoxilin A₃), 5-lipoxygenase [e.g., leukotriene (LT) D₄], and epoxygenase (epoxyeicosatrienoic acids) (675). On the other hand, as shown in Ehrlich ascites tumor cells, swelling stimulates the formation of the leukotrienes, namely, LTD₄ , at the expense of prostaglandins such as prostaglandin (PG) E₂ (675). Both phospholipase A₂ and 5-lipoxygenase are activated by Ca²⁺ (542 675). Thus an increase of intracellular Ca²⁺ concentration during cell swelling could participate in the activation of these two enzymes during cell swelling. Along these lines, LTD₄ may overcome the inhibitory effect of the calmodulin antagonist pimozide on cell volume regulation, suggesting that LTD₄ is a signal downstream of Ca²⁺ (673).

Arachidonic acid has been shown to inhibit glial cell volume regulation (1052) and to inhibit volume regulatory Cl⁻ channels (403 673 679 1047). On the other hand, it may increase Ca²⁺ concentration in renal collecting duct and activate K⁺ channels in neurons (622 1213). Moreover, the 15-lipoxygenase product of arachidonic acid hepoxilin A₃ activates volume regulatory K⁺ channels in platelets (798–801), and the 5-lipoxygenase product LTD₄ activates volume regulatory K⁺ and Cl⁻ channels (547 592 674 675 679) and volume regulatory taurine release (592 678) in Ehrlich ascites tumor cells, as well as taurine release in fish erythrocytes (1207). 5-Lipoxygenase products similarly appear to mediate regulatory cell volume decrease in colonic epithelium (277 281 282), chromaffin cells (287), MDCK cells (947), and human fibroblasts (808). However, in most of these cell types, the evidence comes largely from effects of 5-lipoxygenase inhibitors such as nordihydroguaiaretic acid (NDGA). In Ehrlich ascites tumor cells (679) and proximal renal tubules (Völkl and Lang, unpublished observations), on the other hand, the inhibitory effect of NDGA was not overcome by the addition of LTD₄ , pointing to an additional effect of the drug not related to 5-lipoxygenase inhibition. It may more directly inhibit the volume regulatory Cl⁻ channels (438) or be effective by increasing arachidonic acid concentration (1052).

The enhanced formation of leukotrienes in swollen Ehrlich ascites tumor cells parallels a decreased formation of PGE₂ , an effect possibly accounting for the inhibition of Na⁺ channels (679). Those channels are thought to be stimulated by PGE₂ (679). On the other hand, in ciliary epithelial cells, PGE₂ was thought to mediate the activation of volume regulatory K⁺ channels during cell swelling (191). Prostaglandin E₂ similarly activates K⁺ channels in MDCK cells (1153) and erythrocytes (743).

In collecting duct principal cells, inhibition of phospholipase A₂ with quinacrine blunted the activation of volume regulatory Ca²⁺-sensitive K⁺ channels, which, on the other hand, were activated by arachidonic acid (751). In LLC-PK₁ cells, however, volume regulatory rubidium flux was not modified by arachidonic acid, even though it was inhibited by an arachidonic acid antagonist (262).

Ketoconazole, an inhibitor of epoxygenase (cytochrome P-450), impedes volume regulatory efflux of osmolytes, such as sorbitol, betaine, myo-inositol, or amino acids from renal papillary cells (354), MDCK cells (38), and C6 glioma cells (818 1171). However, the inhibitory effect is not reversed by addition of hydroxyeicosatetraenoic acids (818), indicating that the inhibitory effect on osmolyte flux is not due to inhibition of epoxygenase. Similarly, in Necturus gallbladder, ketoconazole does not prevent regulatory KCl efflux but stimulates NaCl entry, leading to cell swelling (615).

In addition to their influence on volume-sensitive ion channels, phospholipase A₂ and a cytochrome P-450 product of arachidonic acid have been invoked in mediating the swelling-induced cellular release of sorbitol (354).

The fatty acid composition of the cell membrane can be modulated by dietary polyunsaturated fatty acids, which lead to enhanced formation of leukotrienes and thus to acceleration of RVD in Ehrlich ascites tumor cells (712).

L. pH in Acidic Cellular Compartments

As evidenced from acridine orange and fluorescein isothiocyanate-dextran fluorescence, hepatocyte swelling leads to alkalinization of acidic cellular compartments, whereas cell shrinkage enhances the acidity in those compartments (156 683 1088 1089 1279 1280).

The lysosomal proteases are known to have their pH optimum in the acidic range, and alkalinization of the lysosomes is well known to inhibit hepatic proteolysis (859 860). Thus the alkalinizing effect on acidic cellular compartments could at least in theory contribute to the antiproteolytic action of cell swelling. Along these lines, alkalinization of acidic cellular compartments parallels the cell swelling and antiproteolytic effect of transforming growth factor-β1 on LLC-PK₁ cells (752). However, the contribution of vesicular alkalinization to the antiproteolytic effect of cell swelling remains to be proven. At least in liver cells, swelling alkalinizes prelysosomal rather than lysosomal compartments (766 1090). Moreover, inhibition of tyrosine kinase by erbstatin interferes with prelysosomal alkalinization but not with inhibition of proteolysis (S. vom Dahl and D. Häussinger, unpublished observations), pointing to some antiproteolytic mechanisms independent of lysosomal pH.

The alkalinization of acidic cellular compartments in hepatocytes occurs not only if cell swelling is due to decrease of extracellular osmolarity but also if cell swelling is caused by inhibition of K⁺ channels and by concentrative uptake of amino acids (1279).

It appears that the influence of cell volume on pH of acidic cellular compartments is not confined to prelysosomes in hepatocytes but involves a number of distinct compartments in a great variety of cells, such as pancreatic β-cells, glial cells, neurons, vascular smooth muscle cells, proximal renal tubules, MDCK cells, alveolar cells, macrophages, and fibroblasts (153–157 684 1090 1283). Accordingly, the functions of these compartments may be modified by alterations of cell volume.

M. Gene Expression

Both cell swelling and cell shrinkage markedly influence the expression of a wide variety of genes (see Table 1).

**Table 1. Effect of cell volume on gene expression**
Effect	Gene/Gene Product Affected
Cell swelling
+	c-jun in hepatocytes (328)
+	c-fos in cardiac myocytes (1044)
+	JNK-1 in cardiac myocytes (1044)
+	ERK-1,2 in cardiac myocytes (1044)
+	Ornithine decarboxylase in LLC-PK₁ cells (75 769), leukemia cells (977), CHO cells (761), and hepatocytes (1215)
−	TNF-α in macrophages (1392)
+	β-Actin (1202)
+	Tubulin (511)
Cell shrinkage
+	Aldose reductase in MDCK cells and kidney medulla (373 1130)
+	Na⁺-inositol cotransporter SMIT (141 670 1318)
+	Na⁺-betaine cotransporter BGLT1 (319 878 1319 1372 1393)
+	Na⁺-taurine cotransporter (1238 1239 1320 1322)
+	ROSIT, putative osmolyte transporter (1323)
+	Amino acid transport system A (182 380 1135 1373)
+	α₁-Subunit Na⁺-K⁺-ATPase (322)
+	P-glycoprotein (1333)
+	ClC-K1 in kidney (1241)
+	Serine/threonine kinase h-sgk (1295)
+	Egr-1 in MDCK cells (205 206 208) and cardiomyocytes (1361)
+	α₁-Chimerin in neurons (286)
+	c-fos in MDCK cells (208), hypothalamic cells (396), and cardiomyocytes (1361)
+	Heat shock proteins (11 208 1116 1192)
+	Cyclooxygenase-2 (1391)
+	PEPCK (713 886 1317)
−	Tyrosine hydroxylase in PC12 cells (621)
−	Dopamine β-hydroxylase in PC12 cells (621)
+	Tyrosine aminotransferase (1317)
+	Tissue plasminogen activator in endothelial and HeLa cells (733)
+	αβ-Crystallin in lens and kidney (245)
−	Matrix metalloproteinase 9 (1031)
+	Matrix proteins in chondrocytes (1244)
−	Laminin B2 in mesangial cells (603)
+	Vasopressin (866)
+	CD9 antigen in MDCK and PAP-HT25 cells (1115)

+, Stimulation; −, inhibition; CHO, Chinese hamster ovary; TNF-α, tumor necrosis factor-α; MDCK, Madin-Darby canine kidney; PEPCK, phosphoenolpyruvate carboxykinase. For review, see Reference 144. Reference numbers are given in parentheses.

As indicated in section iiC, exposure of cells to enhanced extracellular osmolarity or ionic strength stimulates the expression of aldose reductase and the Na⁺-coupled transport systems for inositol, betaine, taurine, and amino acids. The function of these proteins serves cellular accumulation of osmolytes and thus reestablishes osmotic equilibrium and cell volume constancy (144). Moreover, cell shrinkage stimulates the expression of heat shock proteins that serve to stabilize the proteins and thus to counteract the detrimental effects of increased salt concentrations. The cell volume regulated kinase h-sgk (see sect. iiiH) is a putative element of the signaling cascade triggering cell volume regulation. Furthermore, cell shrinkage stimulates the expression of proteins with diverse functions not obviously related to RVI, such as P-glycoprotein, ClC-K1, and Na⁺-K⁺-ATPase α₁-subunit, cyclooxygenase-2, the GTPase-activating protein for Rac α₁-chimerin, the immediate early gene transcription factors Egr1–1 and c-Fos, vasopressin, phosphoenolpyruvate carboxykinase, tyrosine aminotransferase, tyrosine hydroxylase, dopamine β-hydroxylase, matrix metalloproteinase 9, and several matrix proteins (see Table 1).

Cell swelling similarly stimulates the expression of a variety of proteins including β-actin, tubulin, cyclooxygenase-2, extracellular signal-regulated kinases ERK-1 and ERK-2, JNK, the transcription factors c-Jun and c-Fos, ornithine decarboxylase, and tissue plasminogen activator (see Table 1).

Information on the mechanisms triggering altered gene expression remains scanty (1254). Some evidence points to involvement of the cytoskeleton (76). The expression of aldose reductase is regulated by a distinct osmolarity-responsive element (320 321 1036). The stimulation of c-fos expression by swelling of cardiac myocytes is apparently secondary to tyrosine phosphorylation (1044); the c-jun transcription after swelling of hepatocytes is at least partially the result of MAPK activation, followed by phosphorylation of c-Jun (895 1072 1211). Cell volume changes modify phosphorylation of a histonelike nuclear protein (1057), and hypertonicity has been shown to alter the karyotype (1237).

In mice, a gene (rol) has been identified that renders erythrocytes resistant to osmotic lysis. The product of this gene is likely to be involved in the stimulation of volume regulatory K⁺ fluxes. However, the precise function of this gene remains elusive (318).

IV. CHALLENGES OF CELL VOLUME CONSTANCY

A multitude of mechanisms alter cell volume. They may do so by overriding the volume regulatory mechanims, by knocking them out, or by shifting their volume regulatory set point.

A. Alterations of Extracellular Osmolarity

In mammalian tissues, most cells are exposed to extracellular fluid with well-controlled osmolarity. A notable exception is the kidney medulla, where extracellular osmolarity may approach values exceeding isotonicity by a factor of >4 (1033). Any blood cell passing the kidney medulla experiences exposure to this high ambient osmolarity and subsequent return to isosmolarity within seconds. Medullary cells have not only to cope with this excessive extracellular osmolarity for prolonged periods but encounter rapid changes of osmolarity during transition from antidiuresis to diuresis, when medullary osmolarity rapidly decreases toward isosmolarity (63).

Less dramatic alterations of extracellular osmolarity occur during intestinal absorption, which exposes intestinal cells to anisosmotic luminal fluid and may modify portal blood osmolarity and liver cell volume (460).

Other tissues are exposed to altered extracellular osmolarity during a variety of disorders. Although moderate, these alterations are still highly relevant challenges to cell volume control.

Because Na⁺ salts (mainly NaCl) contribute >90% to extracellular osmolarity, a significant decrease of extracellular osmolarity is necessarily paralleled by hyponatremia. A variety of clinical conditions can lead to hyponatremia (20 21 90 816 905 1265). Hyponatremia may reflect an excess of water, either due to excessive oral load or due to impaired renal elimination, or a deficit of Na⁺ due to renal or extrarenal loss (90 606 1264). In both cases, the hyponatremia reflects a decreased extracellular osmolarity, leading to cell swelling. Excessive water intake is seen in psychiatric disorders (22). Causes for impaired renal water elimination include inappropriate antidiuretic hormone (ADH) secretion, glucocorticoid deficiency, hypothyroidism, and renal and hepatic failure. Renal and/or extrarenal loss of Na⁺ may result from mineralocorticoid deficiency, salt losing kidney, nephrotic syndrome, osmotic diuresis, vomiting, and diarrhea (90). Moreover, a wide variety of drugs including diuretics, cyclooxygenase inhibitors, and certain central nervous system active drugs may lead to hyponatremia due to loss of Na⁺ and/or to retention of water (90). Hyposmolar hyponatremia is further observed after burns, pancreatitis, and crush syndrome (90).

Hyponatremia does not necessarily indicate hyposmolarity but may occur in isosmolar or even hyperosmolar states (90). Extracellular osmolarity may be enhanced despite normal or even decreased extracellular Na⁺ concentration during hyperglycemia in uncontrolled diabetes mellitus (27) and ethanol poisoning (1010). Moreover, hyponatremia cannot be equated with cell swelling. As detailed in section ivF, cell swelling or cell shrinkage may prevail in diabetes mellitus. Burns, pancreatitis, and severe trauma, all conditions associated with hyponatremia (see above), may actually lead to muscle cell shrinkage rather than cell swelling (507).

Extracellular osmolarity is increased in hypernatremia, due to excessive oral intake and/or renal retention of Na⁺ and/or renal and extrarenal loss of water (325 553 858 1142). Causes include excessive sweating, osmotic diuresis, lack of ADH or defective renal response to ADH, and drinking of seawater (553).

Even though extracellular osmolarity increases due to accumulation of urea in uremia (803), urea easily passes cell membranes and does thus not usually cause osmotic gradients across the cell membrane. Nevertheless, as shown in several cell types, high extracellular urea concentrations may trigger cell shrinkage by modifying the set point for volume regulatory mechanisms (see sect. iiiA). Cell shrinkage may be the signal for increase of osmolyte concentration in the brain, which has been observed to parallel enhanced urea concentration in uremia (1223).

Rapid correction of chronically enhanced osmolarity may lead to cell swelling, namely, to cerebral edema (28 1157). Chronic increases of extracellular osmolarity are compensated by cells through accumulation of osmolytes, which may not be rapidly readjusted. Cerebral betaine, inositol, and glycerophosphorylcholine, for instance, may remain enhanced for days after correction of extracellular hypertonicity (746 1208). Conversely, rapid correction of hyponatremia may prove similarly harmful (1141 1156).

B. Alterations of Extracellular Ion Composition

Even at constant extracellular osmolarity, cell volume constancy may be challenged by altered extracellular ion composition (see Table 2).

Most importantly, an increase of extracellular K⁺ concentration depolarizes the cell membrane and eventually leads to cellular uptake of K⁺ with accompanying anions (mainly Cl⁻ and HCO⁻₃) and subsequent cell swelling. Conversely, a decrease of extracellular K⁺ could result in cell shrinkage due to cellular loss of KCl (see Table 2).

An increase of extracellular HCO⁻₃ concentration could swell cells by electrogenic entry, hyperpolarization, reduced driving force for K⁺ exit, and subsequent accumulation of KHCO₃ (976). During correction of extracellular acidosis in the course of the treatment of diabetic ketoacidosis, increasing extracellular pH allows the cells to extrude H⁺ through the Na⁺/H⁺ exchanger, similarly leading to cell swelling (1255).

Several organic anions such as acetate, lactate, and proprionate swell cells by entry of the unionized acid, intracellular dissociation, stimulation of Na⁺/H⁺ exchange by cytosolic acidosis, and subsequent accumulation of Na⁺ and organic anions (see Table 2). A similar effect is exerted by CO₂ . In general, acidosis favors cell swelling, whereas cellular alkalosis has the opposite effect (see Table 2). Along these lines, the cellular accumulation of lactate in muscle exercise triggers volume regulatory mechanisms (1048).

Isotonic replacement of Cl⁻ with gluconate leads to cell shrinkage due to cellular loss of Cl⁻ (and K⁺) (see Table 2).

C. Energy Depletion

As pointed out in section iiB, the maintenance of a constant cell volume requires the expenditure of energy to fuel the Na⁺-K⁺-ATPase, which is required to establish the ionic gradients across the cell membrane. Inhibition of Na⁺-K⁺-ATPase by ouabain or during ischemia eventually leads to cell swelling. In cardiac myocytes, the swelling is preceded by transient cell shrinkage due to increase of intracellular Ca²⁺ and hypercontraction (31 174 1131).

As would be expected, ischemia leads to swelling of the brain (347 1229) by impairment of Na⁺-K⁺-ATPase and subsequent accumulation of NaCl (347 593). However, according to in vitro studies on glial and neuronal cells, energy depletion alone does not result in cell swelling (35 613 775 1396). Rather, additional factors such as the intracellular acidosis (91 578 611 1299) may account for cell swelling observed during ischemia (625). Furthermore, cell swelling in cerebral ischemia is favored by an increase of extracellular K⁺ concentration (612) and by extracellular accumulation of glutamate (42 1396), which stimulates cationic channels through N-methyl-d-aspartate (NMDA) receptors and leads to subsequent accumulation of Na⁺, depolarization, and uptake of Cl⁻ (185 186). In the heart, recovery from ischemia is facilitated in the presence of the Na⁺/H⁺ exchange inhibitor 3-methylsulfonyl-4-piperidinobenzoyl-guanidine-mesilate (HOE-694) (1085).

Alterations of cell volume are encountered during cryopreservation of organs (366 394 681). Low temperatures inhibit the Na⁺-K⁺-ATPase and may thus be expected to eventually result in cell swelling.

D. Ion Transport Altered by Hormones and Transmitters

As listed in Table 2, a wide variety of hormones has been shown to alter cell volume.

Most importantly, insulin swells hepatocytes by activation of both Na⁺/H⁺ exchange and Na⁺-K⁺-2Cl⁻ cotransport (4 472 953), and glucagon shrinks hepatocytes, presumably by activation of ion channels (473 1286 1287). The effect of these hormones on cell volume accounts for several of the effects on hepatocyte metabolism (504 506 1286 1287). It should be pointed out that insulin and glucagon modify cell volume at hormone concentrations well encountered under physiological conditions. This is not necessarily true for all hormones listed in Table 2. Similar to insulin, several growth factors increase cell volume in a variety of cells by stimulation of Na⁺/H⁺ exchange and in some cases of Na⁺-K⁺-2Cl⁻ cotransport (see Table 2). An increase of cell volume appears to be required for cell proliferation (see sect. vI).

Activation of Na⁺ channels or nonselective cation channels by excitatory neurotransmitters such as glutamate tends to swell neurons, whereas activation of K⁺ channels or anion channels by inhibitory neurotransmitters such as GABA tends to shrink neurons (see Table 2).

Secretagogues may stimulate transepithelial transport by enhancing cellular ion entry, ion exit, or both. If stimulation of ion entry prevails, the cells swell, whereas if ion exit is preferentially activated, the cells shrink. Thus secretagogues may either swell (e.g., epinephrine) or shrink (e.g., acetylcholine) the cells (see Table 2).

In kidney medulla, ADH enhances extracellular osmolarity and thus forces the medullary cells to accumulate osmolytes (1033 1075). Furthermore, ADH may more directly trigger the formation or accumulation of osmolytes (880).

E. Substrate Transport

The transport and cellular accumulation of amino acids lead to cell swelling (Table 2). Especially Na⁺-coupled transport processes can generate large chemical gradients across the cell membrane, due to the steep electrochemical gradient for Na⁺. For instance, cellular glutamine has been observed to increase by >30 mM after the addition of 3 mM glutamine to portal blood (502).

As listed in Table 2, transport of several other substrates such as glucose, taurine, and taurocholeate similarly increases cell volume.

F. Metabolism

In theory, any reaction resulting in an increase of osmotically active substances, such as degradation of proteins to amino acids, glycogen to glucose phosphate, or triglycerides to glycerol and fatty acids, may be expected to create intracellular osmolarity. However, very little is known about the influence of metabolism on cell volume.

Exercising muscle may lead to cellular accumulation of lactate and thus may increase cell volume (1048). The developing intracellular acidosis may compound cell swelling by activation of the Na⁺/H⁺ exchanger.

Diabetic ketoacidosis may cause cell swelling (125 197 646 1388) due to cellular uptake of acids and enhanced Na⁺/H⁺ exchange activity in compensation for cellular H⁺ generation (1255). More importantly, high glucose concentrations favor cellular formation and accumulation of sorbitol through aldose reductase (143 180 559 748 990 1196). As a consequence, cells decrease other osmolytes such as myo-inositol (143 411 1079 1158 1222 1386 1387), an effect which can be reversed by inhibition of aldose reductase with sorbinil (303 326 1218). On the other hand, hyperglycemia is paralleled by hyperosmolarity, which shrinks cells. In fact, some evidence points to shrinkage of polymorphonuclear lymphocytes in hyperosmolar diabetes mellitus (269).

In addition to creating osmotically active substances, metabolic pathways may alter cell volume indirectly through modification of transport processes across the cell membrane. For instance, a decrease of cellular ATP could activate ATP-sensitive K⁺ channels and thus shrink susceptible cells, a possibility which has, however, not yet been explored. On the other hand, the cellular formation of peroxides has been shown to shrink hepatocytes due to activation of K⁺ channels at the cell membrane (1045). Peroxides similarly activate K⁺ channels in pancreatic β-cells (652) and vascular smooth muscle cells (651) but inhibit N-type K⁺ channels in lymphocytes (1183) and minK channels (152), which are expressed in a variety of cells (150). In endothelial cells, peroxides inhibit Na⁺-K⁺-2Cl⁻ cotransport (305). However, the consequences on cell volume have not been tested in any of those cells.

G. Others

In addition to hormones, a great number of drugs and toxins lead to cell swelling or cell shrinkage (Table 2). For most substances, the functional significance of the effect on cell volume has not been explored.

In several stress situations, such as surgical intervention (306), acute pancreatitis (1027), severe injury, burns, and sepsis (79), a decrease of muscle intracellular space has been observed, leading to disinhibition of proteolysis and thus to hypercatabolism (507). However, the mechanisms underlying muscle cell shrinkage have not yet been elucidated.

V. ROLE OF CELL VOLUME REGULATORY MECHANISMS IN CELL FUNCTIONS

A. Erythrocyte Function

Erythrocyte volume and shape are important determinants of blood viscosity. Cell volume regulatory mechanisms are specifically important in limiting alterations of cell volume during their passage through the hypertonic kidney medulla and during HCO⁻₃ transport in the lung and the periphery. One disorder exacerbated by altered erythrocyte cell volume regulatory mechanisms is sickle cell anemia, where mutations of the hemoglobin chain (HbS) favor the polymerization of deoxygenated hemoglobin, leading to characteristic changes of cell shape (sickling) and impaired deformability of the erythrocytes (591 737); the consequence is a severe increase of blood viscosity (591). The polymerization of hemoglobin is highly dependent on protein concentration and thus on cell volume (297 298). In HbS erythrocytes, volume regulatory KCl cotransport (133 163 164 343 1276) is enhanced, partially due to direct interaction with the mutated hemoglobin (914). Furthermore, cell shrinkage is presumably favored by enhanced activity of Ca²⁺-sensitive K⁺ channels (105 134 343) due to increase of intracellular Ca²⁺ concentration. The ensuing cell shrinkage further favors the polymerization of hemoglobin (591). The expression of the Na⁺/H⁺ exchanger is enhanced, possibly in compensation for cell shrinkage (165). Similarly, cell volume is decreased in homozygous hemoglobin C disease (135).

B. Epithelial Transport

Transcellular ion transport in epithelia is accomplished by entry mechanisms across one cell membrane and ion exit mechanisms at the other cell membrane. Obviously, the entry or extrusion of osmotically active substances during epithelial transport represents a continuous challenge to cell volume constancy.

In intestine, gallbladder, and renal proximal tubules (see Fig. 1A), the luminal uptake of substrates for Na⁺-coupled transport, such as glucose or amino acids, tends to swell the cells, leading to volume regulatory activation of K⁺ channels in the basolateral cell membrane (67 68 122 173 355 493 687 692 706 782 995 1092–1096 1230). The activation of these channels not only limits cell swelling but maintains the electrical driving force for continued transport.

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In the NaCl-reabsorbing thick ascending limb of Henle's loop and diluting segment of the amphibian kidney, NaCl entry is accomplished by luminal Na⁺-K⁺-2Cl⁻ cotransport, basolateral Cl⁻ channels, and Na⁺-K⁺-ATPase as well as apical and basolateral K⁺ channels (416 900 1178). Inhibition of Na⁺-K⁺-ATPase leads to rapid cell swelling, which is prevented by inhibition of luminal Na⁺-K⁺-2Cl⁻ cotransport (444 520 1178). On the other hand, stimulation of transport by ADH involves a well-coordinated increase of transport rate across both luminal and basolateral cell membranes (521) without any appreciable increase of cell volume (519). If the cells are shrunk by increased extracellular osmolarity, they do not display RVI unless they are stimulated with ADH or cAMP (520 522 1177). The hormone not only activates luminal Na⁺-K⁺-2Cl⁻ cotransport but also a Na⁺/H⁺ exchanger in the basolateral cell membrane, which contributes to ion accumulation during RVI (520 522 1177).

Potassium secretion in dark vestibular cells (see Fig. 1B) and stria vascularis marginal cells of the inner ear is accomplished by basolateral Na⁺-K⁺-2Cl⁻ cotransport, Na⁺-K⁺-ATPase, and Cl⁻ channels as well as apical minK channels (1311). The K⁺ channels are activated by cell swelling (1120 1312), and the basolateral Na⁺-K⁺-2Cl⁻ cotransport by cell shrinkage (1315). Cell volume couples the two cell membranes, since excess Na⁺-K⁺-2Cl⁻ cotransport would swell the cells and thus activate the apical K⁺ channels, and excess K⁺ channel activity would shrink the cell and thus turn on Na⁺-K⁺-2Cl⁻ cotransport. Moreover, exposure of the basolateral side to a hypotonic medium stimulates transepithelial transport (1312), possibly by decreasing intracellular Cl⁻ and subsequent activation of Na⁺-K⁺-2Cl⁻ cotransport.

In tight epithelia reabsorbing Na⁺, such as urinary bladder, Na⁺ entry through luminal Na⁺ channels is similarly coordinated with Na⁺-K⁺-ATPase and K⁺ channels at the basolateral cell membrane (179 329 742 789 995 1232 1233 1303 1349). Accordingly, inhibition of the Na⁺-K⁺-ATPase in toad urinary bladder leads to parallel inhibition of luminal Na⁺ channels, preventing luminal Na⁺ entry and cell swelling (252).

In several tight epithelia, insertion of Na⁺ channels was stimulated by decrease of extracellular osmolarity (1231 1347), a function obviously serving Na⁺ homeostasis rather than cell volume regulation.

Activation of K⁺ and Cl⁻ channels during stimulation of secretion in several epithelia (Fig. 1C) may lead to cell shrinkage due to cellular KCl loss (229 338 339 873 1363). Shrinkage then turns on volume regulatory Na⁺/H⁺ exchange and/or Na⁺-K⁺-2Cl⁻ cotransport, which may partially recover cell volume and at the same time supply the cell with further Cl⁻ for secretion (341 549 796 797).

Thus, during both reabsorption of Na⁺ and substrates and secretion of Cl⁻, cell volume participates in the coupling of the basolateral and luminal cell membrane, the so-called cross-talk between the opposing cell membranes (995). It should be kept in mind, however, that cell volume participates in, but does not fully account for, the coupling of the cell membranes (687). Accordingly, even though osmotic cell swelling mimics many effects of swelling induced by substrate transport, the underlying mechanisms are not necessarily identical. For instance, the depolarization resulting from Na⁺-coupled transport alkalinizes the cytosol by impairment of HCO⁻₃ exit (687), whereas osmotic cell swelling leads to cytosolic acidification (see sect. iiiE). Because K⁺ channels are highly sensitive to cytosolic pH (692), their activation is expected to be different between osmotic and substrate-induced cell swelling. In enterocytes, RVD apparently depends on Ca²⁺ from outside and calmodulin-sensitive K⁺ channels, whereas substrate-induced cell swelling appears to be counterregulated by cellular Ca²⁺ release and subsequent activation of Cl⁻ channels by protein kinase C (782 788).

Volume-mediated activation of transporters not only involves ion channels and ion transporters. As pointed out above, cell shrinkage stimulates the expression and/or activity of Na⁺-coupled transporters for inositol (877), betaine (1242 1372), taurine (1238), and neutral amino acids (182 380 1135 1373). Cell swelling, on the other hand, stimulates cellular release of the above osmolytes and of glutathione (503) and cellular uptake of alanine and glutamine (502 1335) and of taurocholate (469 497). Stimulation of osmolyte flux during alterations of cell volume serves to regulate cell volume rather than transepithelial transport, but entry and/or exit may be polarized (377 480 630 1372), and in the liver, cell swelling indeed stimulates transepithelial transport of taurocholate (469 508) and leukotrienes (1340).

Hyperosmolarity stimulates urea transport (392 393) but inhibits transport of NaCl in inner medullary collecting duct (410) and salivary gland (874).

Stimulation of transport during cell swelling may be the result of insertion of the carriers and/or channels into the cell membrane by exocytosis (114 132 462 497 912 969 1260 1354). Exocytosis may be stimulated by an increase of intracellular Ca²⁺ activity. In lung alveolar type II cells, the increase of intracellular Ca²⁺ concentration due to mechanical stress not only accounts for exocytosis but also for stimulation of surfactant secretion (1354). Protein secretion in seminal vesicles, on the other hand, is inhibited by both hyper- and hypotonic extracellular fluid (554). Exposure of the apical side of the pulmonary epithelium to hypotonic fluid is thought to stimulate the secretion of a humoral factor, leading to bronchodilation (367).

Whether the polarized trafficking of vesicles in epithelia is influenced by cell volume has not yet been explored. The polarized distribution of secretory proteins is modified by an alkalinization of vesicular pH (167 931) and could thus theoretically be sensitive to cell volume. However, the alkalinization of vesicles during cell swelling may be too small to significantly interfere with trafficking.

In addition to its effect on transcellular transport, cell volume has been demonstrated to modify the permeability of tight junctions and thus paracellular transport. However, the reported effects are not consistent (29 111 402 930 962 1348 1384).

C. Regulation of Metabolism

As listed in Table 3, cell volume changes modify a wide variety of metabolic functions. Most importantly, cell swelling favors the synthesis and inhibits the degradation of proteins, glycogen, and to a lesser extent lipids (504 506). Cell shrinkage has the opposite effect. Thus cell swelling can be considered as an anabolic signal, whereas cell shrinkage favors cell catabolism.

**Table 3. Influence of cell volume on metabolism**
Effect	Process Affected
+	Glycogen synthesis in hepatocytes (4 12 50 51 53 455 456 555 819 953) and muscle (762)
−	Glycogenolysis (406 696)
−	Glucose-6-phosphatase activity (409)
+	Glucokinase activity in hepatocytes (1261)
−	Glycolysis in muscle and fibroblasts (196 918)
+	Glycolysis in hepatocytes (953)
	Macrophages and lymphocytes (1366)
+	Lactate uptake in hepatocytes (696)
+	Pentose phosphate shunt in hepatocytes (496 1046)
−	Release of glutamine and alanine from muscle (945)
+	Protein synthesis in hepatocytes (1007 1159), HeLa cells (1008 1343), and mammary cells (825)
−	Proteolysis in hepatocytes (471 472 498 499 767 1284 1285 1287)
+	Amino acid uptake (100 500 502)
+	Glutamine breakdown in liver (502), lymphocytes, and macrophages (1366)
−	Glutamine synthesis (502)
+	Glycine and alanine oxidation (496 510 676)
+	Urea synthesis from amino acids (505)
−	Urea synthesis from NH⁺₄ (500 502)
+	Glutathione (GSH) efflux (503)
−	GSSG release into bile (1046)
+	Ornithine decarboxylase activity and expression (769 1215)
+	RNA and DNA synthesis in HeLa cells (1008)
+	Ketoisocaproate oxidation (510)
+	Acetyl CoA carboxylase (49 51 53 555)
+	Lipogenesis (51)
−	Carnitine palmitoyltransferase I activity (457 841 1389)
+	Taurocholate excretion into bile (469 497 508)
+	Respiration in glial cells (609) and sperm (231)
−	Cellular ATP concentration in hepatocytes (820)
−	Phosphocreatine concentrations in glioma cells (747)
+	Formation of active oxygen species in neutrophils (658 659)
+	Bile secretion (497)

+, Stimulation upon cell swelling and/or inhibition by cell shrinkage; −, inhibition upon cell swelling and/or stimulation by cell shrinkage. For effects on gene expression, see Table 1. For effects on intracellular signaling, see text. Reference numbers are given in parentheses.

In hepatocytes, the influence of cell volume on metabolism is one way that insulin and glucagon exert their metabolic effects. Insulin increases liver cell volume by activation of Na⁺/H⁺ exchange and Na⁺-K⁺-2Cl⁻ cotransport and thus triggers a variety of metabolic functions, including protein and glycogen synthesis and inhibition of protein and glycogen degradation (4 504 506). The effect of insulin on proteolysis is fully accounted for by the cell swelling effect of the hormone. Conversely, glucagon and cAMP stimulate proteolysis and glycogenolysis and inhibit protein synthesis in part by cell shrinkage due to activation of ion channels and subsequent release of KCl (504). Although cell shrinkage correlates well with the inhibitory effect of cAMP and ADH on protein synthesis, this is not true for the effects of insulin and phenylephrine (1159). Thus cell volume may play a less prominent role in hormonal regulation of protein synthesis than in proteolysis. The same probably holds true for glycogen metabolism and lipogenesis.

The antiproteolytic effect of cell swelling depends on an intact microtubule network (156 1284) and could thus not be reproduced in freshly isolated hepatocytes (820), which suffer from a disintegrated microtubule network (511 1284).

The set points of volume regulatory mechanisms and thus cell volume can be altered by a wide variety of other hormones and transmitters, which thus trigger the metabolic pattern typical for swollen or shrunken cells (Table 1). By this means, the mediators exploit volume regulatory mechanisms to exert their effects on cellular metabolism.

In addition to hormones, nutrients may modify protein, glycogen, and lipid metabolism in part through their influence on cell volume. In fact, the antiproteolytic effect of glutamine and glycine in liver has been shown to be completely accounted for by their influence on cell volume (471). The antiproteolytic and swelling effect of glycine is potentiated after starvation (471 1285), which upregulates the glycine transporting system A (515). However, the antiproteolytic action of other amino acids such as phenylalanine, serine, alanine, and proline cannot be fully explained by their effects on cell volume. Thus mechanisms other than cell swelling contribute to the antiproteolytic action of some amino acids.

The influence of cell volume on metabolism is not restricted to macromolecular synthesis and breakdown. Swelling of hepatocytes apparently interferes with the transfer of reducing equivalents through the mitochondrial malate/aspartate shuttle (503). The lack of aspartate impedes the formation of urea from NH₃ , an effect that is overcome by addition of lactate and pyruvate, allowing the mitochondrial regeneration of oxaloacetate (503). The formation of urea from glutamine is enhanced after cell swelling (500).

Some effects of cell swelling caused by a decrease of extracellular osmolarity may actually be due to concomitant mitochondrial swelling (969) because of decreasing ambient osmolarity. Glutamine breakdown (502) and glycine oxidation (510), for instance, are stimulated not only by decrease of extracellular osmolarity but also by glucagon, cAMP, and several Ca²⁺-mobilizing hormones that swell mitochondria (465–467), but at the same time shrink hepatocytes (see Table 2). Similarly, the swelling-induced decrease of the β-hydroxybutyrate-to-acetoacetate ratio (510) is probably due to stimulation of the respiratory chain due to concomitant mitochondrial swelling (274 466).

Peroxides may modify cell volume by activation of ion channels (see Table 2). They shrink hepatocytes by activation of K⁺ channels (470). On the other hand, superoxide has been shown to swell erythrocytes (1247). Cell volume in turn influences the peroxide metabolism; cell swelling stimulates and cell shrinkage inhibits flux through the pentose phosphate pathway and NADPH generation (1046). Thus cell swelling provides NADPH for glutathione reductase to produce reduced glutathione (GSH) and strengthens the protective mechanisms against peroxides (1046). On the other hand, cell swelling should favor the formation of reactive oxygen species by NADPH oxidase, which is inhibited by high osmolarity (1186). Furthermore, components of the cytosolic burst oxidase have been found to be dissociated by high osmolarity (573). Moreover, cell swelling stimulates formation of arachidonic acid (see sect. iiiK), which is required for activation of NADPH oxidase (526). Accordingly, osmotic cell swelling stimulates (602) and osmotic cell shrinkage inhibits formation of peroxides in neutrophils (602 659 795 810).

The enhanced formation of sorbitol in diabetes mellitus (see sect. ivF) has been implicated in the generation of several diabetic complications such as neuropathy, retinopathy, microangiopathy, and cataracts (143). Similarly, the cellular accumulation of galactitol with subsequent decrease of other osmolytes has been implicated in the pathophysiology of galactosemia (80 302). However, the mechanisms linking cell swelling with defined sequelae of diabetes mellitus or galactosemia are far from understood.

Information on metabolic effects of cell volume in mammalian cells other than hepatocytes is still scarce (see Table 3), even though it appears highly unlikely that the influence of altered cell volume on metabolism is restricted to hepatocytes. For instance, mechanical or osmotic deformation of chondrocytes or osteoblasts, respectively, may stimulate the synthesis of proteoglycans and proteins (123 623 1244) and thus foster cartilage and bone growth, which indeed correlated with chondrocyte volume (661). Moreover, a decrease of muscle cell volume was correlated with hypercatabolism in several clinical conditions (507).

Certainly, more experimental information is needed on the interaction of cell volume and cell metabolism in other cells, such as glial cells and adipocytes.

D. Receptor Recycling

The formation of coated pits and internalization of low-density lipoproteins (LDL) and transferrin receptors are inhibited by both increase of extracellular osmolarity (246 485 531 644 909) and K⁺ depletion (485 700 701), both maneuvers expected to shrink cells. Conversely, internalization of LDL or ferritin is increased by hypotonic extracellular fluid (644 707). However, because almost identical effects were exerted by KCl and NaCl but not by glucose or urea, the altered internalization appeared to be due to the ionic strength rather than cell volume (644). Increased ionic strength may impede internalization by interference with the formation of coated pits (531). On the other hand, cell swelling has been shown to inhibit endocytosis (1316).

Cell swelling leads rather to cytosolic acidification (see sect. iiiE), which has been shown to interfere with endocytosis from coated pits (485 530 1056). Moreover, cell swelling reverses lysosomal acidification, which is a prerequisite for normal recycling of LDL (57) and transferrin receptors (248). Accordingly, cell swelling would have been expected to impede receptor recycling. The vesicular alkalinization and cytosolic acidification after cell swelling may not be sufficient to significantly interfere with receptor recycling, and the effects of ionic strength exceed the weak effects of cell volume. The reason for the interference of K⁺ depletion with the formation of coated pits (701) remains, however, unexplained.

In glial cells, NH₃ , which swells the cells (10 897 898) and alkalinizes their lysosomes (153), leads to upregulation of peripheral type benzodiazepine receptors (571 572). Moreover, binding of benzodiazepine to glial cells (570), muscarinic drugs to peritoneal cells (537), atrial natriuretic peptide to collecting duct cells (561), and endothelin to renal cells (1268) increases after hypotonic exposure. Excessive osmotic shrinkage, on the other hand, has been shown to induce clustering and internalization of cytokine receptors and thus to mimic effects of the ligands (1020).

Taken together, these data do not suggest a uniform influence of cell volume as such on the regulation of cell membrane receptors.

E. Hormone and Transmitter Release

An increase in cell membrane tension, as occurs during cell swelling, has been described to trigger fusion of endocytotic vesicles with the plasma membrane, leading to release of vesicle contents and insertion of ion channels in the cell membrane (132 417 462 508 969 1260). The mechanism requires Ca²⁺ and an intact actin filament network. If the same is true for secretory vesicles, osmotic cell swelling should stimulate hormone release (Fig. 2).

**Fig. 2.**Mechanism of stimulated hormone release and of contraction after swelling of endocrine and vascular smooth muscle cells, respectively. Swelling leads to activation of anion channels, and exit of Cl⁻ depolarizes cell membrane. Subsequent activation of voltage-sensitive Ca²⁺ channels stimulates Ca²⁺ entry. Ca²⁺ then triggers hormone release from endocrine cells or contraction of smooth muscle cells, respectively.

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Cell swelling has indeed been shown to trigger the release of insulin (95 768), prolactin (414 1063 1066 1070 1304 1306 1307 1309), gonadotropin-releasing hormone (563), luteinizing hormone (414 415), thyrotropin (414 1065 1306), aldosterone (514 1081–1083 1301), and renin (345 582 1128 1129). Where tested, the hormone-releasing effect was correlated with an increase of intracellular Ca²⁺ activity (514 983 1062 1064–1069 1080 1308). In insulin-secreting β-cells, Ca²⁺ entry during cell swelling is partially due to activation of Cl⁻ channels (82), with subsequent depolarization of the cell membrane and opening of voltage-sensitive Ca²⁺ channels (124).

Osmotic cell shrinkage has been shown to inhibit prolactin release, presumably by inhibiting Ca²⁺ influx (1065 1305). Furthermore, increase of extracellular osmolarity decreases the formation and release of endothelin-1 (640).

For atrial natriuretic factor (ANF), the position is less clear. It is released from cardiac myocytes in response to mechanical stretch (198 1071) and osmotic cell swelling (412). Cell volume may be part of a negative-feedback loop limiting ANF release. Atrial natriuretic factor inhibits the cardiac Na⁺/K⁺/2Cl⁻ exchanger via guanosine 3′,5′-cyclic monophosphate (cGMP), with the resulting cell shrinkage then inhibiting ANF release (199 201). On the other hand, ANF release has been postulated to be stimulated by cell shrinkage (1399 1400).

In contrast to the above hormones, vasopressin is released during cell shrinkage, which apparently leads to disinhibition of a stretch-inactivated cation channel. The activation of this channel leads to depolarization and accelerated action potentials (913). Interestingly, ethanol, which triggers hormone release from other cells (1063 1068), is known to inhibit vasopressin release (90). In addition to ADH, the release of nitric oxide (1152) and of the putative hormones ouabain or ouabainlike factors (98 744) may be stimulated by an increase in plasma osmolarity. Furthermore, hyperosmolarity stimulates the release of histamine from basophil granulocytes (892) and of substance P from C-fiber neurons (375). Alterations of NaCl concentrations have further been shown to modify transmitter release from various regions of the brain (551).

Renin secretion is inhibited by an increase of intracellular Ca²⁺ activity, the so-called Ca²⁺ paradox of renin secretion (461 923). It has been suggested that an increase of intracellular Ca²⁺ activity activates Ca²⁺-sensitive Cl⁻ channels, thus leading to cellular loss of KCl and cell shinkage, which in turn would inhibit renin release (665).

Cell volume may further modify hormone and transmitter release through pH changes in secretory vesicles. In pancreatic β-cells, for instance, acidic proteases within the acidic secretory granules cleave proinsulin to yield insulin, a function probably compromised by cell swelling and fostered by cell shrinkage. Furthermore, the release of insulin may be modified by the luminal pH of the secretory granules and thus be sensitive to alterations of cell volume. In neurons, metabolism, uptake, and release of neurotransmitters may be modified by the luminal pH of synaptic vesicles. For instance, the uptake of neurotransmitters such as catecholamines, glutamate, GABA, and acetylcholine into small synaptic vesicles is driven by a proton gradient between the cytosol and the acid lumen (254). Uptake of glutamate and aspartate into glial cells has indeed been found to be impaired by osmotic cell swelling (628).

Transmitter metabolism may be further influenced by cell volume through effects on the expression of enzymes. At enhanced extracellular K⁺, an increase of extracellular osmolarity inhibits the expression of tyrosine hydroxylase and dopamine β-hydroxylase in PC12 cells (621). Increasing extracellular osmolarity at low extracellular K⁺ was, however, without effect on the expression of these enzymes (621).

Some of the osmolytes released during cell swelling of neurons such as glutamate (148 304 523 550 865 1339), aspartate (550 891), GABA (774 891), glycine (891), and taurine (184 560) function as neurotransmitters in the brain. Hyperosmolar glucose or sorbitol concentrations inhibited K⁺-induced GABA release and inhibited K⁺-induced release of norepinephrine and serotonin (327).

F. Excitability and Contraction

After swelling of cardiac cells, volume-sensitive Cl⁻ currents have been shown to depolarize the cell membrane (1253 1394), enhance excitability, and reduce the duration of the action potential (1139). On the other hand, moderate osmotic shrinkage exerts a positive inotropic effect in the heart (74 432). This latter effect may be due to a direct influence on the contractile elements. As shown in skinned muscle fibers, increased ionic strength destabilizes the actinomyosin complex, thus interfering with the Ca²⁺-activated force (41 398). To the extent that cell shrinkage leads to increase of intracellular ionic strength, this effect could modify muscular contraction. Osmotic swelling of smooth muscle cells (see Fig. 2) activates a depolarizing anion conductance, leading to depolarization, opening of voltage-gated Ca²⁺ channels, increase of intracellular Ca²⁺ activity, and contraction (685). Conversely, osmolar cell shrinkage leads to vasodilation (1112 1152).

An enhanced activity of Na⁺/H⁺ exchanger with resulting cell swelling has been implicated in the generation of one type of essential hypertension (271 314 348 558 664 793 887–889 1022–1024 1026 1109 1124 1330 1390). On the one hand, cell swelling should increase contractility of smooth muscle cells, and on the other hand, enhanced Na⁺/H⁺ exchange activity should favor cell proliferation and thus hypertrophy of vascular smooth muscle cells. Proliferation of vascular smooth muscle cells has been shown to be stimulated by mechanical stretch (770 979).

Neuronal excitability could be affected in several ways by cell volume. Any release of K⁺ for cell volume regulation should enhance extracellular K⁺, decrease the K⁺ equilibrium potential, and thus depolarize the cell membrane. Possibly, however, swollen neurons do not volume regulate by rapid release of electrolytes (23).

As discussed in section vE, glutamate, aspartate, GABA, glycine, and taurine serve both as osmolytes and as neurotransmitters. When released from swollen cells, they may modify the function of neighboring cells (628 1059). Conversely, the osmosensitive betaine transporter transports GABA at higher affinity than betaine (1374). Moreover, sensitivity of neurons to neurotransmitters may be modified by cell volume. For instance, NMDA receptors have been found to be mechanosensitive (929). Cell volume changes may further interfere with neuronal excitability by modifying the pH and trafficking of secretory vesicles (see above). Increases of osmolarity have been shown to increase the percentage of slow miniature end-plate potentials (1262).

Chloride concentration in neurons is regulated by furosemide-sensitive Na⁺-K⁺-2Cl⁻ cotransport (45 839). Activation of K⁺ and Cl⁻ channels shrinks the cells by KCl loss, decreases intracellular Cl⁻ concentration, and thus dissipates the Cl⁻ gradient. The cell shrinkage activates the Na⁺-K⁺-2Cl⁻ cotransport, which not only restores cell volume but also maintains intracellular Cl⁻ activity. Accordingly, GABA-induced depolarization was rendered transient by addition of furosemide (45). Moreover, furosemide has been shown to block synchronized burst discharges in hippocampal slices (538).

Excitability of neurons critically depends on glial cell function (612). One of the major tasks of glial cells is to maintain constancy of extracellular K⁺. Because of the minimal extracellular space, any release of K⁺ from neurons during depolarization would lead to rapid increase of extracellular K⁺ concentration, a dissipation of the chemical K⁺ gradient, and thus to impairment of repolarization. Glial cells accumulate K⁺ and thus blunt the increase of extracellular K⁺ concentration in part by uptake of K⁺ through Na⁺-K⁺-2Cl⁻ cotransport in parallel with Na⁺-K⁺-ATPase (1298). This function is expected to be compromised during glial cell swelling. Glial cell swelling has indeed been implicated in a wide variety of disorders affecting the brain (505 624 649 650 896 898 1220). In hepatic encephalopathy, for instance, the enhanced NH₃ concentration forces the formation and cellular accumulation of glutamine, leading to glial cell swelling (218 896 898). One of the consequences is cellular loss of inositol (218 649 1021). Accordingly, inhibition of glutamine synthetase has been found to be protective against hepatic encephalopathy (512). A striking increase of brain inositol is observed in Alzheimer's disease (1122). It is not clear, though, whether this change relates to altered cell volume regulation and contributes to the pathophysiology of this disease.

In part as a result of the above interactions, increased plasma osmolarity decreases and reduced plasma osmolarity increases the susceptibility to epileptic seizures (22 921). It must be kept in mind, though, that alterations of plasma osmolarity primarily create an osmotic gradient across the blood-brain barrier, leading to respective changes of extracellular space (235 1125) and movements of electrolytes from or to brain tissue (822). The decrease of extracellular space during osmotic cell swelling may be a major cause for altered excitability (921 1224).

**Fig. 3.**Polarized cell volume regulatory ion transport in migrating cells. Cell migrates from left to right. At rear end, oscillations of intracellular Ca²⁺ activity (Ca_i) lead to activation of Ca²⁺-sensitive K⁺ channels, favoring regulatory cell volume decrease (RVD). At leading edge, Na⁺/H⁺ exchange and Na⁺-K⁺-2Cl⁻ cotransport favor regulatory cell volume increase (RVI). Ca²⁺ oscillations further trigger depolymerization of actin filaments at rear end. Fragments are transported to leading edge, where polymerization of actin filaments prevails.

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G. Migration

Migration involves substantial reorganization of the cytoskeleton both at the leading edge and the rear of the cell (202 215 1162) (see Fig. 3). At the leading edge, polymerization of actin filaments prevails, whereas at the rear of the cells, actin filaments are depolymerized (1162). The depolymerization is mediated by capping or escort proteins, such as gelsolin, which are stimulated by Ca²⁺ (237 492 1162 1355). In fact, after chemotactic stimuli, Ca²⁺ concentration increases primarily at the rear of the cell (136 463 756). Bound to the capping or escort proteins, the actin fragments travel toward the leading edge, where they are reutilized for elongation of the actin filaments. The elongation is stimulated by polyphosphoinositides, which bind and thus neutralize the capping proteins (1162). The addition of new elements to the actin filament is thought to be facilitated by protrusion of the cell membrane, which may be caused by local osmotic swelling (1162).

Migration of leukocytes can be stimulated by chemoattractants such as formylpeptides (727). N-formyl-methionyl-leucyl-phenylalanine (FMLP) stimulates Na⁺/H⁺ cotransport in neutrophils, leading to cell swelling (842 870 871 1003 1019 1365). Activation of Na⁺/H⁺ exchange and cell swelling are required for migration, which is impeded by inhibitors of the carrier and osmotic cell shrinkage (1003 1019). Similarly, inhibition of Na⁺-K⁺-2Cl⁻ cotransport with bumetanide inhibited migration of transformed MDCK cells (1101). In those cells, migration further requires the operation of Ca²⁺-sensitive K⁺ channels, which are activated by oscillating intracellular Ca²⁺ activity (240 1101). Inhibition of these channels similarly prevented migration. It is attractive to postulate that migration involves RVD with Ca²⁺ oscillations and activation of K⁺ channels at the rear and RVI with activation of Na⁺/H⁺ exchange and/or Na⁺-K⁺-2Cl⁻ cotransport at the leading edge of a migrating cell. The migration would require asymmetrical distribution and/or activation of channels and carriers. As a matter of fact, the Na⁺/H⁺ exchanger is concentrated at the leading edge (431) and K⁺ channel activity at the rear of the cell (1099 1100), and a Ca²⁺ gradient has been observed within a migrating cell with highest values at the rear (136 401 463 1098).

The elongation of the neuritic cylinder, but not the extension of the growth cone of neurons, has been observed to be stimulated by a decrease of extracellular osmolarity (117). Accordingly, the role of osmotic gradients in the protrusion of the leading edge is still a matter of debate (117 965 1162). Obviously, variation of extracellular osmolarity does more than modify the detachment of the cell membrane from the cytoskeleton. In any case, more experimentation is needed to elucidate the role of cell volume regulatory mechanisms in the machinery of migration.

H. Pathogen Host Interactions

Reports on the interplay of cell volume and infection are scarce. It is well known that cholera toxin activates both Cl⁻ and K⁺ channels via cAMP (337), an effect expected to result in cell shrinkage. The heat-stable toxin from Escherichia coli has been shown to activate Cl⁻ channels via cGMP (749), and erythrocytes infected with malaria display new ion permeation pathways (633). Moreover, several bacteria produce porins, which may be inserted into the host cell membrane (97 771 1328). Because porins may function as Cl⁻ channels (1035 1338), it is tempting to speculate that they serve to alter host cell volume. Exposure of erythrocytes to Schistosoma mansoni membrane fractions has indeed been shown to produce marked cell shrinkage (1201). However, whether the metabolic alterations triggered by cell swelling or shrinkage are favorable for the pathogen is similarly unknown. As outlined above, cell shrinkage inhibits O⁻₂ formation in neutrophils, an effect possibly contributing to the inhibitory effect on bacterial killing in a hypertonic environment (481). On the other hand, a hypertonic environment increases adherence and invasion of Salmonella typhi (1195).

Similar scanty information is available on the role of cell volume in viral infection. The M₂ protein of influenza virus serves as an ion channel (974). Whether the insertion of this channel into the host membrane alters cell volume is not known. Tacaribe virus infection was shown to inhibit Na⁺-K⁺-ATPase (996), and vaccinia virus infection of HeLa cells led to increases of Na⁺ at the expense of K⁺ (899). Infection of fibroblasts with herpes simplex virus leads to profound cell swelling (441). Cell swelling was enhanced in the presence of the antiviral drug 3′-azido-3′-deoxythymidine, which inhibits I_Cln , the putative volume regulatory Cl⁻ channel (441). Infection of renal tubule cells with simian virus 40 results in the appearance of K⁺ channels (1199). Changes in cell volume, on the other hand, may influence viral replication. For instance, a decrease of extracellular NaCl has been shown to reduce replication of reticuloendotheliosis (93) and Sindbis virus (1290) as well as maturation of poliovirus (5). Furthermore, infection of MDCK cells with vesicular stomatitis virus is impaired by increasing extracellular K⁺ at the expense of Na⁺ (7), a maneuver known to induce cell swelling (see Table 2). The effect could not be explained by altered intracellular Ca²⁺ activity but was assumed to be secondary to a depolarization of the cell membrane (7). In duck hepatocytes, increase of extracellular osmolarity markedly reduced duck hepatitis B virus DNA, mRNA, and protein (904). Because shrinkage of hepatocytes leads to depolarization (406), the effect could have been due to either depolarization or cell shrinkage.

In tracheal epithelium, sulfation and sialation of membrane proteins has been shown to be sensitive to luminal pH of acidic cellular compartments, and it has been argued that defective acidification of these compartments in cystic fibrosis leads to altered sulfation and sialation and thus to enhanced adhesion of Pseudomonas aeruginosa (54). Because the primary defect of cystic fibrosis leads to impaired Cl⁻ channel activity (92 170 171 350 1118 1336 1337) and impairment of cell volume regulation (1252), it may be paralleled by cell swelling, which increases lysosomal pH (see sect. iiiL). Thus cell swelling could enhance adhesion of P. aeruginosa and infection, a possibility, however, not yet explored.

Clearly, the role of cell volume in the interaction of host and pathogen is far from understood. The data available thus far, however, are sufficiently intriguing to justify additional experimental effort.

I. Cell Proliferation

A wide variety of mitogenic factors (for review, see Ref. 1000) activate the Na⁺/H⁺ exchanger, and many factors stimulate Na⁺-K⁺-2Cl⁻ cotransport (85 428 826 844 928 1000 1274 1275 1291 1292 1293). One expected consequence of the activation of these transport systems is an increase of cell volume.

Cell proliferation has indeed been shown to correlate with increases of cell volume in fibroblasts (694 695 824 960), mesangial cells (1371), lymphocytes (284 285 454 1114 1117), HL-60 cells (120 146), GAP A3 hybridoma cells (884), smooth muscle cells (317 881), and HeLa cells (1185). As shown for fibroblasts, the cell volume increase parallels the entry of fibroblasts from the G₁ into the S phase (960), which is accompanied by inhibition of K⁺ channels (253). Moreover, large variations of volume regulatory Cl⁻ channels have been observed in ascidian embryos (1273).

Osmotic alterations of cell volume indeed modify cell proliferation. Hypertonic shrinkage inhibits (9 533 840 967 1008 1380) and slight osmotic cell swelling has been shown to accelerate (18) cell proliferation. When exposed to enhanced extracellular ionic strength, the cells may overcome cell shrinkage by cellular accumulation of osmolytes which then allows them to proliferate normally (720 1379 1380).

As illustrated in Figure 4, Ras oncogene expression in fibroblasts is paralleled by enhanced Na⁺/H⁺ exchange and Na⁺-K⁺-2Cl⁻ cotransport activity, leading to an increase of cell volume (694 695 824). The increase of cell volume is related to oscillations of intracellular Ca²⁺ activity (242), which can be triggered by bradykinin, bombesin, or serum in those cells (686 694 697 1296 1359 1360). The Ca²⁺ oscillations cause rapid transient cell shrinkage due to activation of Ca²⁺-sensitive K⁺ channels (1005 1358), followed by a sustained increase of cell volume presumably due to a depolymerization of the actin filaments (243 1004) and subsequent shift of the set point for cell volume regulation (242). The Ca²⁺ oscillations are in turn favored by cell shrinkage (1006), pointing to a negative-feedback loop (Fig. 4).

**Fig. 4.**Cell volume in proliferating cells. Cellular mechanisms triggered by expression of ras oncogene leading to activation or inhibition of cell volume regulatory mechanisms. Expression of Ras oncogene (RAS) sensitizes phospholipase C (PLC) for growth promotors such as bradykinin, bombesin, or serum. As a result, bradykinin-induced formation of inositol 1,4,5-trisphosphate (IP₃) and inositol 1,3,4,5-tetrakisphosphate (IP₄) is enhanced. Instead of a single release of cellular Ca²⁺, bradykinin induces sustained oscillations of intracellular Ca²⁺ concentration by triggering both Ca²⁺ entry through Ca²⁺ channels and Ca²⁺ release from cellular stores. On one hand, Ca²⁺ oscillations cause repetitive activation of Ca²⁺-sensitive K⁺ channels, leading to oscillations of cell membrane potential and transient decrease of cell volume. On the other hand, Ca²⁺ oscillations lead to depolymerization of actin filaments, which presumably facilitates activation of Na⁺/H⁺ exchanger and Na⁺-K⁺-2Cl⁻ cotransport. Activation of these carriers results in uptake of KCl and NaCl. Because Na⁺ is replaced by K⁺ by action of Na⁺-K⁺-ATPase, cells accumulate mainly KCl. Ion uptake increases cell volume, which is one prerequisite for stimulation of cell proliferation. Increase of cell volume is limited by inhibition of Na⁺/H⁺ exchanger and Na⁺-K⁺-2Cl⁻ cotransport by cell swelling (ICS and ECS stand for intracellular and extracellular space, respectively).

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Apparently, the activation of Na⁺/H⁺ exchange and Na⁺-K⁺-2Cl⁻ cotransport is required for stimulation of cell proliferation by ras oncogene (694 697 824 1000). In several cell types, cell proliferation is similarly correlated with enhanced Ca²⁺ and K⁺ channel activity (for review, see Ref. 1000) and is impeded by respective channel inhibitors (17 726 739 893 981 1091 1123 1199 1256 1369). However, the activity of certain ion channels and transporters may not always be required for cell proliferation to occur. Inhibition of the Na⁺/H⁺ exchanger, for instance, is not always found to interfere with cell proliferation (83 189 598 827 1025).

How alterations of cell volume interact with cell cycle control is not known. As outlined above, cell swelling stimulates the protein kinases ERK-1 and ERK-2 (1072), proteins probably involved in regulation of cell cycle (113).

In proliferating cells, the role of increased cell volume in altering further volume-sensitive cellular functions such as alkalinization of lysosomal vesicles (588), decreased proteolysis (501), and increased LDL receptor expression at the cell surface (1136) has not yet been explored.

In contrast to cell proliferation, cell differentiation is accompanied by cell shrinkage in erythroleukemia cells (264 458 607 725), HL-60 leukemic cells (311 475), and EMT6/ro mouse mammary sarcoma cells (118). HL-60 cells shrink despite enhanced expression of Na⁺/H⁺ exchanger (986), which displays altered kinetic properties (227 228). On the other hand, senescent fibroblasts have been shown to gain cell volume (960 961).

J. Cell Death

Apoptotic cell death (617 1367) is triggered by a wide variety of factors including stimulation of specific receptors at the cell membrane, such as the receptor for Fas (CD95) (1074) or tumor necrosis factor-α (655).

One of the hallmarks of apoptotic cell death is cell shrinkage (1 207). Shrinkage may in some cells be secondary to increased intracellular Ca²⁺ activity (922 1226) and subsequent activation of Ca²⁺-sensitive K⁺ and/or Cl⁻ channels. Accordingly, it could be inhibited by K⁺ channel blockers or increased extracellular K⁺ concentration (55 61). Stimulation of the Fas-receptor leads to rapid activation of cell volume regulatory Cl⁻ channels (I. Szabo, E. Gulbins, and F. Lang, unpublished observations) as well as delayed taurine release, the latter effect paralleling cell shrinkage (686a). The loss of cell volume may be functionally important, since a doubling of extracellular osmolarity has been shown to trigger apoptosis (109 811). Moreover, the ability of cells to resist osmotic shrinkage by cell volume regulation paralleled their resistance to apoptosis after an osmotic shock (109). As discussed in section iiiH, osmotic stress triggers the MAPK pathway, leading to activation of JNK via the MAPK kinase (MKK4) (809 853 1020 1216). Both JNK and p38 kinase, another target of MKK4, have been invoked in the triggering of apoptosis (1368). On the other hand, MKK4 has been postulated to protect from apoptosis (894). Thus the precise function of these kinases in apoptosis remains elusive. Whether the proteolytic effect of cell shrinkage (see Table 1) contributes to apoptosis remains to be tested.

Surprisingly, Fas-induced cell death is inhibited during exposure of the cells to moderately hypertonic extracellular fluid (451). Moreover, in lymphocytes, stimulation of the Fas receptor leads to inhibition of the n-type K⁺ channel or Kv1.3 via tyrosine phosphorylation (449 1183), which is the volume regulatory K⁺ channel in lymphocytes (273). It appears that cell shrinkage interferes at some point with the signaling cascade of apoptotic cell death. Fas-induced cell death is triggered by activation of caspases with subsequent stimulation of sphingomyelinases, ceramide formation, activation of Ras, PI 3-kinase, Rac, MKK4, and JNK or p38 kinase (446 448 1368). In addition, activation of Rac triggers formation of active oxygen species (AOS), presumably by the NADPH oxidase (447). Cell shrinkage apparently does not interfere with the cascade leading to Ras activation but prevents the formation of AOS, since the decrease of GSH is blunted in shrunken lymphocytes (451).

Several mechanisms could mediate the inhibition of the signaling cascade: cell shrinkage stimulates the expression of α₁-chimerin (see Table 1), a GTPase activating protein for Rac. If a similar protein is expressed in lymphocytes as a function of cell volume, it could account for some inhibition of NADP oxidase activity. Moreover, cell shrinkage inhibits glucose flux through the pentose phosphate pathway, decreasing the availability of NADPH (see sect. vC). Furthermore, hyperosmolarity interferes with the respiratory burst oxidase (573). Along these lines, hyperosmotic cell shrinkage blunts agonist-triggered AOS formation (602 659 795 810), and hyposmotic cell swelling stimulates AOS formation (602) in polymorphonuclear leukocytes. Leukocyte AOS production through NADPH oxidase is further inhibited by high concentrations of urea (1187), which at least in some cells leads to cell shrinkage (see sect. iiiA) and similar to osmotic shrinkage inhibits Fas-induced cell death (E. Gulbins and F. Lang, unpublished observations).

Although the decreased NADPH availability in shrunken cells may interfere with endogenous formation of AOS and thus protects from Fas-induced cell death, it renders the cells more vulnerable to exogenous oxidative stress, whereas cell swelling appears to protect from exogenous oxidative stress (804 1046).

Beyond the role of AOS, cell shrinkage is expected to turn on Na⁺/H⁺ exchange, leading to alkalinization (see sect. iiB). Intracellular acidosis, on the other hand, has been considered a prerequisite for apoptosis (405).

Because cell shrinkage apparently interferes with the Fas signaling pathway, the inhibition of K⁺ channels after activation of the Fas receptor could serve to prevent premature inhibition of the signaling cascade by cell shrinkage. In analogy with Fas-induced cell death, methylprednisolone-induced apoptosis of thymocytes was observed to be inhibited by low doses of the K⁺ ionophore valinomycin (255). Furthermore, tumor necrosis factor-α has been shown to stimulate Na⁺/H⁺ exchange (1248).

Clearly, the role of cell volume regulatory mechanisms in apoptotic cell death is still ill-defined, and at this point, their functional significance remains a matter of speculation.

K. Others

Obviously, a number of further functions involve alterations of cell volume and/or activation of volume regulatory mechanisms.

Phagocytosis, for instance, could be expected to increase cell volume. Indeed, phagocytotic Kupffer cells do contain betaine, which is released during phagocytosis (1319 1393). Similarly, the ion channels activated during phagocytosis (641) may at least in part serve RVD. Moreover, phagocytosis has been shown to be sensitive to ambient osmolarity (1321).

Activation of thrombocytes is paralleled by excessive cell shrinkage, which participates in the metamorphosis of the cells (59).

Furthermore, some evidence points to the involvement of cell volume regulatory mechanisms during lymphocyte adhesion, which may play a permissive role in the activation of Na⁺/H⁺ exchange (562 1103–1106). Binding to L-selectins, with the receptors mediating the first contact of lymphocytes with the endothelial cell surface (1018), triggers an intracellular cascade involving Ras activation (121), ultimately leading to an increase of cell volume (E. Gulbins, B. Brenner, and F. Lang, unpublished observations). The functional significance of these events is still elusive but may relate to the considerable mechanical forces operative during adhesion of lymphocytes to the endothelial surface (1395).

REFERENCES

1 ADEBODUN F., POST J. F. M.¹⁹F NMR studies of changes in membrane potential and intracellular volume during dexamethasone-induced apoptosis in human leukemic cell lines.J. Cell. Physiol.1541993199206
Crossref | PubMed | ISI | Google Scholar
2 ADRAGNA N. C., FONSECA P., LAUF P. K.Hydroxyurea affects cell morphology, cation transport, and red blood cell adhesion in cultured vascular endothelial cells.Blood831994553560
PubMed | ISI | Google Scholar
3 AGIUS, L., M. PEAK, and M. AL-HABORI. What determines the increase in liver cell volume in the fasted-to-fed transition: glycogen or insulin? Biochem. J. 276: 843–845, 1991.
Google Scholar
4 AGIUS L., PEAK M., BERESFORD G., AL-HABORI M., THOMAS T. H.The role of ion content and cell volume in insulin action.Biochem. Soc. Trans.221994516522
Crossref | PubMed | ISI | Google Scholar
5 AGOL V. I., LIPSKAYA G. Y., TOLSKAYA E. A., VOROSHILOVA M. K., ROMANOVA L. I.Defect in poliovirus maturation under hypotonic conditions.Virology411970533540
Crossref | PubMed | ISI | Google Scholar
6 AGRE P., BROWN D., NIELSEN S.Aquaporin water channels: unanswered questions and unresolved controversies.Curr. Opin. Cell. Biol.71995472483
Crossref | PubMed | ISI | Google Scholar
7 AKESON M., SCHARFF J., SHARP C. M., NEVILLE D. M.Jr. Evidence that plasma membrane electrical potential is required for vesicular stomatitis virus infection of MDCK cells: a study using fluorescence measurements through polycarbonate support.J. Membr. Biol.12519928191
Crossref | PubMed | ISI | Google Scholar
8 AKTORIES K., HALL A.Botulinum ADP-ribosyltransferase C₃: a new tool to study low molecular weight GTP-binding proteins.Trends Pharmacol. Sci.101989415418
Crossref | PubMed | ISI | Google Scholar
9 ALBERTYN J., HOHMANN S., THEVELEIN J. M., PRIOR B. A.GPD1, which encodes glycerol-3-phosphate dehydrogenase, is essential for growth under osmotic stress in Saccharomyces cerevisiae, and its expression is regulated by the high-osmolarity glycerol response pathway.Mol. Cell. Biol.14199441354144
Crossref | PubMed | ISI | Google Scholar
10 ALBRECHT J., BENDER A. S., NORENBERG M. D.Ammonia stimulates the release of taurine from cultured astrocytes.Brain Res.6601994288292
Crossref | PubMed | ISI | Google Scholar
11 ALFIERI R., PETRONINI P. G., URBANI S., BORGHETTI A. F.Activation of heat shock transcription factor 1 by hypertonic shock in 3T3 cells.Biochem. J.3191996601606
Crossref | PubMed | ISI | Google Scholar
12 AL-HABORI M., PEAK M., THOMAS T. H., AGIUS L.The role of cell swelling in the stimulation of glycogen synthesis by insulin.Biochem. J.2821992789796
Crossref | PubMed | ISI | Google Scholar
13 ALPER S. L., PALFREY H. C., DERIEMER S. A., GREENGARD P.Hormonal control of protein phosphorylation in turkey erythrocytes. Phosphorylation by cAMP-dependent and Ca²⁺-dependent protein kinases of distinct sites in goblin, a high molecular weight protein of the plasma membrane.J. Biol. Chem.25519801102911039
PubMed | ISI | Google Scholar
14 ALTENBERG G. A., DEITMER J. W., GLASS D. C., REUSS L.P-glycoprotein-associated Cl⁻ currents are activated by cell swelling but do not contribute to cell volume regulation.Cancer Res.541994618622
PubMed | ISI | Google Scholar
15 ALTENBERG G. A., VANOYE C. G., HAN E. S., DEITMER J. W., REUSS L.Relationships between rhodamine 123 transport, cell volume, and ion-channel function of P-glycoprotein.J. Biol. Chem.269199471457149
PubMed | ISI | Google Scholar
16 ALVAREZ-LEEFMANS F. J., GAMINO S. M., REUSS L.Cell volume changes upon sodium pump inhibition in Helix aspersa neurones.J. Physiol. (Lond.)4581992603619
Crossref | Google Scholar
17 AMIGORENA S., CHOQUET D., TEILLAUD J. L., KORN H., FRIDMAN W. H.Ion channel blockers inhibit B cell activation at a precise stage of the G₁ phase of the cell cycle. Possible involvement of K⁺ channels.J. Immunol.144199020382045
PubMed | ISI | Google Scholar
18 ANBARI K., SCHULTZ R. M.Effect of sodium and betaine in culture media on development and relative rates of protein synthesis in preimplantation mouse embryos in vitro.Mol. Reprod. Dev.3519932428
Crossref | PubMed | ISI | Google Scholar
19 ANDERSON, P. M. Purification and properties of the glutamine- and N-acetyl-l-glutamate-dependent carbamoyl phosphate synthetase from liver of Squalus acanthias. J. Biol. Chem. 256: 12228–12238, 1981.
Google Scholar
20 ANDERSON R. J.Hospital-associated hyponatremia.Kidney Int.29198612371247
Crossref | PubMed | ISI | Google Scholar
21 ANDERSON R. J., CHUNG H. M., KLUGE R., SCHRIER R. W.Hyponatremia: a prospective analysis of its epidemiology and the pathogenetic role of vasopressin.Ann. Intern. Med.1021985164168
Crossref | PubMed | ISI | Google Scholar
22 ANDREW R. D.Seizure and acute osmotic change: clinical and neurophysiological aspects.J. Neurol. Sci.1011991718
Crossref | PubMed | ISI | Google Scholar
23 ANDREW R. D., LOBINOWICH M. E., OSEHOBO E. P.Evidence against volume regulation by cortical brain cells during acute osmotic stress.Exp. Neurol.1431997300312
Crossref | PubMed | ISI | Google Scholar
24 ANDREW R. D., MACVICAR B. A.Imaging cell volume changes and neuronal excitation in the hippocampal slice.Neuroscience621994371383
Crossref | PubMed | ISI | Google Scholar
25 ANDREWS M. A., MAUGHAN D. W., NOSEK T. M., GODT R. E.Ion-specific and general ionic effects on contraction of skinned fast-twitch skeletal muscle from the rabbit.J. Gen. Physiol.98199111051125
Crossref | PubMed | ISI | Google Scholar
26 ARAKAWA T., TIMASHEFF S. N.The stabilization of proteins by osmolytes.Biophys. J.471985411414
Crossref | PubMed | ISI | Google Scholar
27 ARIEFF A. I., CARROLL H. J.Nonketotic hyperosmolar coma with hyperglycemia: clinical features, pathophysiology, renal function, acid-base balance, plasma cerebrospinal fluid equilibria and the effects of therapy in 37 cases.Medicine5119727394
Crossref | PubMed | ISI | Google Scholar
28 ARIEFF A. I., KLEEMAN C. R.Cerebral edema in diabetic comas. II. Effects of hyperosmolarity, hyperglycemia and insulin in diabetic rabbits.J. Clin. Endocrinol. Metab.38197410571067
Crossref | PubMed | ISI | Google Scholar
29 ARMITAGE W. J., JUSS B. K., EASTY D. L.Response of epithelial (MDCK) cell junctions to calcium removal and osmotic stress is influenced by temperature.Cryobiology311994453460
Crossref | PubMed | ISI | Google Scholar
30 ARORA P. D., BIBBY K. J., McCULLOCH C. A. G.Slow oscillations of free intracellular calcium ion concentration in human fibroblasts responding to mechanical stretch.J. Cell. Physiol.1611994187200
Crossref | PubMed | ISI | Google Scholar
31 ASKENASY N., TASSINI M., VIVI A., NAVON G.Intracellular volume measurement and detection of edema: multinuclear NMR studies of intact rat hearts during normothermic ischemia.Magn. Reson. Med.331995515520
Crossref | PubMed | ISI | Google Scholar
32 AUNIS D., BADER M. F.The cytoskeleton as a barrier to exocytosis in secretory cells.J. Exp. Biol.1391988253266
PubMed | ISI | Google Scholar
33 AYRAPETYAN S. N., SULEYMANIAN M. A.On the pump-induced cell volume changes.Comp. Biochem. Physiol. A Physiol.641979571575
Crossref | ISI | Google Scholar
34 BACK J. F., OAKENFULL D., SMITH M. B.Increased thermal stability of proteins in the presence of sugars and polyols.Biochemistry18197951915196
Crossref | PubMed | ISI | Google Scholar
35 BAETHMANN A., KEMPSKI O.Ischemic brain edema.Prog. Appl. Microcirc.1319893853
Crossref | Google Scholar
36 BAGNARA A. S., McDONALD L. E., SLADE H. M.Deoxyadenosine toxicity in an adenosine deaminase-inhibited human CCRF-CEM T-lymphoblastoid cell line causes cell swelling.Biochim. Biophys. Acta11801992163172
Crossref | PubMed | ISI | Google Scholar
37 BAGNASCO S., BALABAN R., FALES H. M., YANG Y.-M., BURG M. B.Predominant osmotically active organic solutes in rat and rabbit renal medullas.J. Biol. Chem.261198658725877
PubMed | ISI | Google Scholar
38 BAGNASCO S. M., MONTROSE M. H., HANDLER J. S.Role of calcium in organic osmolyte efflux when MDCK cells are shifted from hypertonic to isotonic medium.Am. J. Physiol.264(Cell Physiol. 33)1993C1165C1170
Link | Google Scholar
39 BAGNASCO S. M., MURPHY H. R., BEDFORD J. J., BURG M. B.Osmoregulation by slow changes in aldose reductase and rapid changes in sorbitol flux.Am. J. Physiol.254(Cell Physiol. 23)1988C788C792
Link | Google Scholar
40 BAGNASCO S. M., UCHIDA S., BALABAN R. S., KADOR P. F., BURG M. B.Induction of aldose reductase and sorbitol in renal inner medullary cells by elevated extracellular NaCl.Proc. Natl. Acad. Sci. USA84198717181720
Crossref | PubMed | ISI | Google Scholar
41 BAGNI M. A., CECCHI G., GRIFFITHS P. J., MAEDA Y., RAPP G., ASHLEY C. C.Lattice spacing changes accompanying isometric tension development in intact single muscle fibers.Biophys. J.67199419651975
Crossref | PubMed | ISI | Google Scholar
42 BAKER A. J., ZOHRNOW M. H., SHELLER M. S., YAKSH T. L., SKILLING S. R., SMULLIN D. H., LARSON A. A., KUCZENSKI R.Changes in extracellular concentrations of glutamate, aspartate, glycine, dopamine, serotonin, and dopamine metabolites after transient global ischemia in the rabbit brain.J. Neurochem.57199113701379
Crossref | PubMed | ISI | Google Scholar
43 BAKKER-GRUNWALD T.Potassium permeability and volume control in isolated rat hepatocytes.Biochim. Biophys. Acta7311983239242
Crossref | PubMed | ISI | Google Scholar
44 BALABAN R. S., BURG M. B.Osmotically active organic solutes in the renal inner medulla.Kidney Int.311987562564
Crossref | PubMed | ISI | Google Scholar
45 BALLANYI K., GRAFE P.Cell volume regulation in the nervous system.Renal Physiol. Biochem.111988142157
PubMed | Google Scholar
46 BALLANYI K., GRAFE P., SERVE G., SCHLUE W. R.Electrophysiological measurements of volume changes in Leech neuropile glial cells.Glia31990151158
Crossref | PubMed | ISI | Google Scholar
47 BALLATORI N., TRUONG A. T., JACKSON P. S., STRANGE K., BOYER J. L.ATP depletion and inactivation of an ATP-sensitive taurine channel by classic ion channel blockers.Mol. Pharmacol.481995472476
PubMed | ISI | Google Scholar
48 BANDERALI U., ROY G.Activation of K⁺ and Cl⁻ channels in MDCK cells during volume regulation in hypotonic media.J. Membr. Biol.1261992219234
Crossref | PubMed | ISI | Google Scholar
49 BAQUET A., GAUSSIN V., BOLLEN M., STALMANS W., HUE L.Mechanism of activation of liver acetyl-CoA carboxylase by cell swelling.Eur. J. Biochem.217199310831089
Crossref | PubMed | Google Scholar
50 BAQUET A., HUE L., MEIJER A. J., VAN WOERKOM G. M., PLOMP P. J. A. M.Swelling of rat hepatocytes stimulates glycogen synthesis.J. Biol. Chem.2651990955959
PubMed | ISI | Google Scholar
51 BAQUET A., LAVOINNE A., HUE L.Comparison of the effects of various amino acids on glycogen synthesis, lipogenesis and ketogenesis in isolated rat hepatocytes.Biochem. J.27319915762
Crossref | PubMed | ISI | Google Scholar
52 BAQUET A., MEIJER A. J., HUE L.Hepatocyte swelling increases inositol 1,4,5-trisphosphate, calcium and cyclic AMP concentration but antagonizes phosphorylase activation by Ca²⁺-dependent hormones.FEBS Lett.2781991103106
Crossref | PubMed | ISI | Google Scholar
53 BAQUET A., MAISIN L., HUE L.Swelling of rat hepatocytes activates acetyl-CoA carboxylase in parallel to glycogen synthase.Biochem. J.2781991887890
Crossref | PubMed | ISI | Google Scholar
54 BARASCH J., KISS B., PRINCE A., SAIMAN L., GRUENERT D., AL-AWQATI Q.Defective acidification of intracellular organelles in cystic fibrosis.Nature35219917073
Crossref | PubMed | ISI | Google Scholar
55 BARBIERO G., DURANTI F., BONELLI G., AMENTA J. S., BACCINO F. M.Intracellular ionic variations in the apoptotic death of L cells by inhibitors of cell cycle progression.Exp. Cell Res.2171995410418
Crossref | PubMed | ISI | Google Scholar
56 BAROIN A., GARCIA-ROMEU F., LAMARRE T., MOTAIS R.A transient sodium-hydrogen exchange system induced by catecholamines in erythrocytes of rainbow trout, Salmo gairdneri.J. Physiol. (Lond.)35619842131
Crossref | Google Scholar
57 BASU S. K., GOLDSTEIN J. L., ANDERSON R. G. W., BROWN M. S.Monensin interrupts the recycling of low density lipoprotein receptors in human fibroblasts.Cell241981493502
Crossref | PubMed | ISI | Google Scholar
58 BAUDOUIN-LEGROS M., ASDRAM L., TONDELIER D., PAULAIS M., ANAGNOSTOPOULOS T.Extracellular urea concentration modulates cAMP production in the mouse MTAL.Kidney Int.5019962633
Crossref | PubMed | ISI | Google Scholar
59 BAUER, C., and W. WUILLEMIN. Blood, plasma proteins, coagulation, fibrinolysis, and thrombocyte function. In: Comprehensive Human Physiology, edited by R. Greger and U. Windhorst. Berlin: Springer-Verlag, 1996, p. 1651–1677.
Google Scholar
60 BEAR C. E., PETERSON O. H.l-Alanine evokes opening of single Ca²⁺-activated K⁺ channels in rat liver cells.Pflügers Arch.4101987342344
Crossref | PubMed | ISI | Google Scholar
61 BEAUVAIS F., MICHEL L., DUBERTRET L.Human eosinophils in culture undergo a striking and rapid shrinkage during apoptosis. Role of K⁺ channels.J. Leukoc. Biol.571995851855
Crossref | PubMed | ISI | Google Scholar
62 BECK F.-X., DÖRGE A., RICK R., THURAU K.Intra- and extracellular element concentrations of rat renal papilla in antidiuresis.Kidney Int.251984397403
Crossref | PubMed | ISI | Google Scholar
63 BECK F.-X., DÖRGE A., THURAU K.Cellular osmoregulation in renal medulla.Renal Physiol. Biochem.111988174186
PubMed | Google Scholar
64 BECK F.-X., SCHMOLKE M., GUDER W. G.Osmolytes.Curr. Opin. Nephrol. Hypertens.119924352
Crossref | PubMed | Google Scholar
65 BECK F.-X., SCHMOLKE M., GUDER W. G., DÖRGE A., THURAU K.Osmolytes in renal medulla during rapid changes in papillary tonicity.Am. J. Physiol.262(Renal Fluid Electrolyte Physiol. 31)1992F849F856
Google Scholar
66 BECK F.-X., SONE M., DÖRGE A., THURAU K.Effect of increased distal sodium delivery on organic osmolytes and cell electrolytes in the renal outer medulla.Pflügers Arch.4221992233238
Crossref | PubMed | ISI | Google Scholar
67 BECK J. S., BRETON S., MAIRBAURL H., LAPRADE R., GIEBISCH G.Relationship between sodium transport and intracellular ATP in isolated perfused rabbit proximal convoluted tubule.Am. J. Physiol.261(Renal Fluid Electrolyte Physiol. 30)1991F634F639
Google Scholar
68 BECK J. S., LAPRADE R., LAPOINTE J. Y.Coupling between transepithelial Na transport and basolateral K conductance in renal proximal tubule.Am. J. Physiol.266(Renal Fluid Electrolyte Physiol. 35)1994F517F527
Google Scholar
69 BECK J. S., POTTS D. J.Cell swelling, cotransport activation and potassium conductance in isolated perfused rabbit kidney proximal tubules.J. Physiol. (Lond.)4251990369378
Crossref | Google Scholar
70 BEDFORD J. J., BAGNASCO S. M., KADOR P. F., HARRIS H. W.Jr., and M. B. BURG. Characterization and purification of a mammalian osmoregulatory protein, aldose reductase, induced in renal medullary cells by high extracellular NaCl.J. Biol. Chem.26219871425514259
PubMed | ISI | Google Scholar
71 BENDER A. S., NEARY J. T., BLICHARSKA J., NORENBERG L. O., NORENBERG M. D.Role of calmodulin and protein kinase C in astrocytic cell volume regulation.J. Neurochem.58199218741882
Crossref | PubMed | ISI | Google Scholar
72 BENDER A. S., NEARY J. T., NORENBERG M. D.Role of phosphoinositide hydrolysis in astrocyte volume regulation.J. Neurochem.61199315061514
Crossref | PubMed | ISI | Google Scholar
73 BENDER A. S., NORENBERG M. D.The role of K⁺ influx on glutamate induced astrocyte swelling: effect of temperature.Acta Neurochir.6019942830
Google Scholar
74 BEN HAIM, S. A., Y. EDOUTE, G. HAYAM, and O. S. BETTER. Sodium modulates inotropic response to hyperosmolarity in isolated working rat heart. Am. J. Physiol. 263 (Heart Circ. Physiol. 32): H1154–H1160, 1992.
Google Scholar
75 BENIS R. C., LUNDGREN D. W.Sodium-dependent co-transported analogues of glucose stimulate ornithine decarboxylase mRNA expression in LLC-PK₁ cells.Biochem. J.2891993751756
Crossref | PubMed | ISI | Google Scholar
76 BEN-ZE'EV A.Animal cell shape changes and gene expression.Bioessays131991207212
Crossref | PubMed | ISI | Google Scholar
77 BERDIEV B. K., PRAT A. G., CANTIELLO H. F., AUSIELLO D. A., FULLER C. M., JOVOV B., BENOS D. J., ISMAILOV I. I.Regulation of epithelial sodium channels by short actin filaments.J. Biol. Chem.27119961770417710
Crossref | PubMed | ISI | Google Scholar
78 BERGH C., KELLEY S. J., DUNHAM P. B.K-Cl cotransport in LK sheep erythrocytes: kinetics of stimulation by cell swelling.J. Membr. Biol.1171990177188
Crossref | PubMed | ISI | Google Scholar
79 BERGSTRÖM J. P., LARSSON J., NORDSTRÖM H., VINNARS E., ASKANAZI J., ELWYN D. H., KINNEY J. M., FÜRST P. J.Influence of injury and nutrition on muscle water and electrolytes: effect of severe injury, burns and sepsis.Acta Chir. Scand.1531987261266
PubMed | Google Scholar
80 BERRY G. T.The role of polyols in the pathophysiology of hypergalactosemia.Eur. J. Pediatr.154, Suppl.1995S53S64
Crossref | ISI | Google Scholar
81 BERRY G. T., MALLEE J. J., KWON H. M., RIM J. S., MULLA W. R., MUENKE M., SPINNER N. B.The human osmoregulatory Na⁺/myo-inositol cotransporter gene (SLC5A3): molecular cloning and localization to chromosome 21.Genomics251995507513
Crossref | PubMed | ISI | Google Scholar
82 BEST L., MILEY H. E., YATES A. P.Activation of an anion conductance and beta cell depolarization during hypotonically induced insulin release.Exp. Physiol.811996927933
Crossref | PubMed | ISI | Google Scholar
83 BESTERMAN J. M., TYREY S. J., CRAGOE E. J.Jr., and P. CUATRECASAS. Inhibition of epidermal growth factor-induced mitogenesis by amiloride and an analog: evidence against a requirement for Na⁺/H⁺ exchange.Proc. Natl. Acad. Sci. USA81198467626766
Crossref | PubMed | ISI | Google Scholar
84 BEYENBACH, K. W. (Editor). Cell Volume Regulation. Comparative Physiology, edited by R. K. H. Kinne and E. Kinne-Saffran. Basel: Karger, 1990, vol. 4.
Google Scholar
85 BIANCHINI, L., and S. GRINSTEIN. Regulation of volume-modulating ion transport systems by growth promoters. In: Advances in Comparative and Environmental Physiology, edited by F. Lang and D. Häussinger. Berlin: Springer-Verlag, 1993, vol. 14, p. 249–270.
Google Scholar
86 BIANCHINI L., KAPUS A., LUKACS G., WASAN S., WAKABAYASHI S., POUYSSEGUR J., YU F. H., ORLOWSKI J., GRINSTEIN S.Responsiveness of mutants of NHE-1 isoform of the Na⁺/H⁺ antiport to osmotic stress.Am. J. Physiol.269(Cell Physiol. 38)1995C998C1007
Link | Google Scholar
87 BIANCHINI L., POUYSSEGUR J.Molecular structure and regulation of vertebrate Na⁺/H⁺ exchangers.J. Exp. Biol.196199433745
PubMed | ISI | Google Scholar
88 BIANCHINI L., WOODSIDE M., SARDET C., POUYSSEGUR J., TAKAI A., GRINSTEIN S.Okadaic acid, a phosphatase inhibitor, induces activation and phosphorylation of the Na⁺/H⁺ antiport.J. Biol. Chem.26619911540615413
PubMed | ISI | Google Scholar
89 BIBBY K. J., McCULLOCH C. A. G.Regulation of cell volume and [Ca²⁺]_i in attached human fibroblasts responding to anisosmotic buffers.Am. J. Physiol.266(Cell Physiol. 35)1994C1639C1649
Link | Google Scholar
90 BICHET, D. G., R. KLUGE, R. L. HOWARD, and R. W. SCHRIER. Hyponatremic states. In: The Kidney: Physiology and Pathophysiology (2nd ed.), edited by D. W. Seldin and G. Giebisch. New York: Raven, 1992, p. 1727–1751.
Google Scholar
91 BICKLER P. E.Cerebral anoxia tolerance in turtles: regulation of intracellular calcium and pH.Am. J. Physiol.263(Regulatory Integrative Comp. Physiol. 32)1992R1298R1302
Google Scholar
92 BIJMAN J., QUINTON P. M.Influence of abnormal Cl⁻ impermeability on sweating in cystic fibrosis.Am. J. Physiol.247(Cell Physiol. 16)1984C3C9
Link | Google Scholar
93 BISHOP J. M., MALDONADO R. L., GARRY R. F., ALLEN P. T., BOSE H. R., WAITE M. R. F.Effect of medium of lowered NaCl concentration on virus release and protein synthesis in cells infected with reticuloendotheliosis virus.J. Virol.171976446452
PubMed | ISI | Google Scholar
94 BIZE I., DUNHAM P. B.Staurosporine, a protein kinase inhibitor, activates K-Cl cotransport in LK sheep erythrocytes.Am. J. Physiol.266(Cell Physiol. 35)1994C759C770
Link | Google Scholar
95 BLACKARD W. G., KIKUCHI M., RABINOVITCH A., RENOLD A. E.An effect of hyposmolarity on insulin release in vitro.Am. J. Physiol.2281975706713
Link | ISI | Google Scholar
96 BLACKWELL J. R., GILMOUR D. J.Physiological response of the unicellular green alga Chlorococcum submarinum to rapid changes in salinity.Arch. Microbiol.15719918691
Crossref | ISI | Google Scholar
97 BLAKE, M. S., and E. C. GOTSCHLICH. Functional and immunological properties of pathogenic Neisseria surface proteins. In: Bacterial Outer Membranes as Model Systems, edited by M. Inouye. New York: Wiley, 1987, p. 377–400.
Google Scholar
98 BLAUSTEIN M. P.Physiological effects of endogenous ouabain: control of intracellular Ca²⁺ stores and cell responsiveness.Am. J. Physiol.264(Cell Physiol. 33)1993C1367C1387
Link | Google Scholar
99 BLUMENFELD J. D., HEBERT S. C., HEILIG C. W., BALSCHI J. A., STROMSKI M. E., GULLANS S. R.Organic osmolytes in inner medulla of Brattleboro rat: effects of ADH and dehydration.Am. J. Physiol.256(Renal Fluid Electrolyte Physiol. 25)1989F916F922
Google Scholar
100 BODE B. P., KILBERG M. S.Amino acid-dependent increase in hepatic system N activity is linked to cell swelling.J. Biol. Chem.266199173767381
PubMed | ISI | Google Scholar
101 BOE R., GJERTSEN B. T., VINTERMYR O. K., HOUGE G., LANOTTE M., DOSKELAND S. O.The protein phosphatase inhibitor okadaic acid induces morphological changes typical of apoptosis in mammalian cells.Exp. Cell Res.1951991237246
Crossref | PubMed | ISI | Google Scholar
102 BOESE S. H., WEHNER F., KINNE R. K. H.Taurine permeation through swelling activated anion conductance in rat IMCD cells in primary culture.Am. J. Physiol.271(Renal Fluid Electrolyte Physiol. 40)1996F498F507
Google Scholar
103 BONANNO J. A.K⁺-H⁺ exchange, a fundamental cell acidifier in corneal epithelium.Am. J. Physiol.260(Cell Physiol. 29)1991C618C625
Link | Google Scholar
104 BONDY C. A., LIGHTMAN S. L.Developmental and physiological regulation of aldose reductase mRNA expression in renal medulla.Mol. Endocrinol.3198914091416
Crossref | PubMed | Google Scholar
105 BOOKCHIN R. M., ORTIZ O. E., LEW V. L.Activation of calcium-dependent potassium channels in deoxygenated sickled red cells.Prog. Clin. Biol. Res.2401987193200
PubMed | Google Scholar
106 BOOKSTEIN C., MUSCH M. W., DEPAOLI A., XIE Y., RABENAU K., VILEREAL M., RAO M. C., CHANG E. B.Characterization of the rat Na⁺/H⁺ exchanger isoform NHE4 and localization in rat hippocampus.Am. J. Physiol.271(Cell Physiol. 40)1996C1629C1638
Link | Google Scholar
107 BOOKSTEIN C., MUSCH M. W., DEPAOLI A., XIE Y., VILLEREAL M., RAO M. C., CHANG E. B.A unique sodium-hydrogen exchange isoform (NHE-4) of the inner medulla of the rat kidney is induced by hyperosmolarity.J. Biol. Chem.26919942970429709
Crossref | PubMed | ISI | Google Scholar
108 BORON, W. F., E. M. HOGAN, and B. A. DAVIS. Involvement of a G protein in the shrinkage-induced activation of Na-H exchange in barnacle muscle fibres. In: Cellular and Molecular Physiology of Cell Volume Regulation, edited by K. Strange. Boca Raton, FL: CRC, 1994, p. 299–310.
Google Scholar
109 BORTNER C. D., CIDLOWSKI J. A.Absence of volume regulatory mechanisms contributes to the rapid activation of apoptosis in thymocytes.Am. J. Physiol.271(Cell Physiol. 40)1996C950C961
Link | Google Scholar
110 BOSTROM T. E., FIELD M. J., GYORY A. Z., DYNE M., COCKAYNE D. J.Electron probe X- ray microanalysis of intracellular element concentrations in cryosections in the presence of changes in cell volume.J. Microsc.1621991319333
Crossref | PubMed | ISI | Google Scholar
111 BOUCHER R. C.Human airway ion transport (part II).Am. J. Respir. Crit. Care Med.1501994581593
Crossref | PubMed | ISI | Google Scholar
112 BOULANGER Y., LEGAULT P., TEJEDOR A., VINAY P., THERIAULT Y.Biochemical characterization and osmolytes in papillary collecting ducts from pig and dog kidneys.Can. J. Physiol. Pharmacol.66198812821290
Crossref | PubMed | ISI | Google Scholar
113 BOULTON T. G., YANCOPOULOS G. D., GREGORY J. S., SLAUGHTER C., MOOMAW C., HSU J., COBB M. H.An insulin-stimulated protein kinase similar to yeast kinases involved in cell cycle control.Science24919906467
Crossref | PubMed | ISI | Google Scholar
114 BOYER J. L., GRAF J., MEIER P. J.Hepatic transport systems regulating pH_i , cell volume, and bile secretion.Annu. Rev. Physiol.541992415438
Crossref | PubMed | ISI | Google Scholar
115 BRANDI G., ROSSI L., SCHIAVANO G. F., SALVAGGIO L., ALBANO A., MAGNANI M.In vitro toxicity and metabolism of 2′,3′-dideoxycytidine.Chem. Biol. Interact.7919915364
Crossref | PubMed | ISI | Google Scholar
116 BRAUN A. P., SCHULMAN H.A non-selective cation current activated via the multifunctional Ca²⁺-calmodulin-dependent protein kinase in human epithelial cells.J. Physiol. (Lond.)48819953755
Crossref | Google Scholar
117 BRAY D., MONEY N. P., HAROLD F. M., BAMBURG J. R.Responses of growth cones to changes in osmolality of the surrounding medium.J. Cell Sci.981991507515
PubMed | ISI | Google Scholar
118 BREDEL-GEISSLER A., KARBACH U., WALENTA S., VOLLRATH L., MUELLER-KLIESER W.Proliferation associated oxygen consumption and morphology of tumor cells in monolayer and spheroid culture.J. Cell. Physiol.15319924452
Crossref | PubMed | ISI | Google Scholar
119 BREITWIESER G. E., ALTAMIRANO A. A., RUSSELL J. M.Osmotic stimulation of Na⁺-K⁺-Cl⁻ cotransport in squid giant axon is [Cl⁻]_i dependent.Am. J. Physiol.258(Cell Physiol. 27)1990C749C753
Link | Google Scholar
120 BRENNAN J. K., LEE K. S., FRAZEL M. A., KENG P. C., YOUNG D. A.Interactions of dimethyl sulfoxide and granulocyte-macrophage colony stimulating factor on the cell cycle kinetics and phosphoproteins of G₁-enriched HL-60 cells: evidence of early effects on lamin B phosphorylation.J. Cell. Physiol.1461991425434
Crossref | PubMed | ISI | Google Scholar
121 BRENNER B., GULBINS E., SCHLOTTMAN K., KOPPENHÖFER U., BUSCH G. L., WALZOG B., STEINHAUSEN M., COGGESHALL K. M., LINDERKAMP O., LANG F.L-selectin activates the Ras pathway via the tyrosine kinase p56lck.Proc. Natl. Acad. Sci. USA9319961537615381
Crossref | PubMed | ISI | Google Scholar
122 BRETON S., MARSOLAIS M., LAPOINTE J. Y., LAPRADE R.Cell volume increases of physiologic amplitude activate basolateral K and Cl conductances in the rabbit proximal convoluted tubule.J. Am. Soc. Nephrol.7199620722087
PubMed | ISI | Google Scholar
123 BREUR G. J., VANENKEVORT B. A., FARNUM C. E., WILSMAN N. J.Linear relationship between the volume of hypertrophic chondrocytes and the rate of longitudinal bone growth in growth plates.J. Orthop. Res.91991348359
Crossref | PubMed | ISI | Google Scholar
124 BRITSCH S., KRIPPEIT-DREWS P., GREGOR M., LANG F., DREWS G.Effects of osmotic changes in extracellular solution on electrical activity of mouse pancreatic B-cells.Biochem. Biophys. Res. Commun.2041994641645
Crossref | PubMed | ISI | Google Scholar
125 BRIZZOLARA A., BARBIERI M. P., ADEZATI L., VIVIANI G. L.Water distribution in insulin dependent diabetes mellitus in various states of metabolic control.Eur. J. Endocrinol.1351996609615
Crossref | PubMed | ISI | Google Scholar
126 BRODIN B., NIELSEN R.Small transepithelial osmotic gradients affect apical sodium permeability in frog skin.Pflügers Arch.4231993411417
Crossref | PubMed | ISI | Google Scholar
127 BROSNAN J. T., QIAN D.Endotoxin-induced increase in liver mass and hepatocyte volume.Biochem. Soc. Trans.221994529532
Crossref | PubMed | ISI | Google Scholar
128 BROWN A. D.Microbial water stress.Bacteriol. Rev.401976803846
PubMed | Google Scholar
129 BROWN A. D., SIMPSON J.Water relations of sugar-tolerant yeasts: the role of intracellular polyols.J. Gen. Microbiol.721972589591
Crossref | PubMed | Google Scholar
130 BROWN D.Membrane recycling and epithelial cell function.Am. J. Physiol.256(Renal Fluid Electrolyte Physiol. 25)1989F1F12
Google Scholar
131 BROWN G. C.Total cell protein concentration as an evolutionary constraint on the metabolic control distribution in cells.J. Theor. Biol.1531991195203
Crossref | PubMed | ISI | Google Scholar
132 BRUCK R., HADDAD P., GRAF J., BOYER J. L.Regulatory volume decrease stimulates bile flow, bile acid excretion, and exocytosis in isolated perfused rat liver.Am. J. Physiol.262(Gastrointest. Liver Physiol. 25)1992G806G812
Google Scholar
133 BRUGNARA C., BUNN H. F., TOSTESON D. C.Regulation of erythrocyte cation and water content in sickle cell anemia.Science2321986388390
Crossref | PubMed | ISI | Google Scholar
134 BRUGNARA C., DE FRANCESCHI L., ALPER S. L.Inhibition of Ca²⁺-dependent K⁺ transport and cell dehydration in sickle erythrocytes by clotrimazole and other imidazole derivatives.J. Clin. Invest.921993520526
Crossref | PubMed | ISI | Google Scholar
135 BRUGNARA C., KOPIN A. S., BUNN H. F., TOSTESON D. C.Regulation of cation content and cell volume in hemoglobin erythrocytes from patients with homozygous hemoglobin C disease.J. Clin. Invest.75198516081617
Crossref | PubMed | ISI | Google Scholar
136 BRUNDAGE R. A., FOGARTY K. E., TUFT R. A., FAY F. S.Calcium gradients underlying polarization and chemotaxis of eosinophils.Science2541991703706
Crossref | PubMed | ISI | Google Scholar
137 BRUNNER M., SCHRANER E. M., WILD P.Cellular changes in rat parathyroids provoked by progesterone and testosterone.Cell Tissue Res.2681992283286
Crossref | PubMed | ISI | Google Scholar
138 BUCHE A., COLSON P., HOUSSIER C.Organic osmotic effectors and chromatin structure.J. Biomol. Struct. Dyn.81990601618
Crossref | PubMed | ISI | Google Scholar
139 BUCHE A., COLSON P., HOUSSIER C.Effect of organic effectors on chromatin solubility, DNA-histone H1 interactions, DNA and histone H1 structures.J. Biomol. Struct. Dyn.11199395119
Crossref | PubMed | ISI | Google Scholar
140 BURG M. B.Role of aldose reductase and sorbitol in maintaining the medullary intracellular milieu.Kidney Int.331988635641
Crossref | PubMed | ISI | Google Scholar
141 BURG M. B.Molecular basis for osmoregulation of organic osmolytes in renal medullary cells.J. Exp. Zool.2681994171175
Crossref | PubMed | Google Scholar
142 BURG M. B.Molecular basis of osmotic regulation.Am. J. Physiol.268(Renal Fluid Electrolyte Physiol. 37)1995F983F996
Google Scholar
143 BURG M. B., KADOR P. F.Sorbitol, osmoregulation, and the complications of diabetes.J. Clin. Invest.811988635640
Crossref | PubMed | ISI | Google Scholar
144 BURG M. B., KWON E. D., KULTZ D.Osmotic regulation of gene expression.FASEB J.10199615981606
Crossref | PubMed | ISI | Google Scholar
145 BURG M. B., KWON E. D., PETERS E. M.Glycerophosphocholine and betaine counteract the effect of urea on pyruvate kinase.Kidney Int.50, Suppl.1996S100S104
ISI | Google Scholar
146 BURGER C., WICK M., BRUSSELBACH S., MULLER R.Differential induction of “metabolic genes” after mitogen stimulation and during normal cell cycle progression.J. Cell Sci.1071994241252
PubMed | ISI | Google Scholar
147 BURGOYNE R. D., CHEEK T. R.Reorganisation of peripheral actin filaments as a prelude to exocytosis.Biosci. Rep.71987281288
Crossref | PubMed | ISI | Google Scholar
148 BURNASHEV N.Recombinant ionotropic glutamate receptors: functional distinctions imparted by different subunits.Cell. Physiol. Biochem.31993318331
Crossref | ISI | Google Scholar
149 BURNHAM C. E., BUERK B., SCHMIDT C., BUCUVALAS J. C.A liver specific isoform of the betaine/GABA transporter in the rat: cDNA sequence and organ distribution.Biochim. Biophys. Acta1284199648
Crossref | PubMed | ISI | Google Scholar
150 BUSCH A. E., MAYLIE J.MinK channels: a minimal channel protein with a maximal impact.Cell. Physiol. Biochem.31993270276
Crossref | ISI | Google Scholar
151 BUSCH A. E., VARNUM M., ADELMAN J. P., NORTH R. A.Hypotonic solution increases the slowly activating potassium current IsK expressed in Xenopus oocytes.Biochem. Biophys. Res. Commun.1841992804810
Crossref | PubMed | ISI | Google Scholar
152 BUSCH A. E., WALDEGGER S., HERZER T., RABER G., GULBINS E., TAKUMI T., MORIYOSHI K., NAKANISHI S., LANG F.Molecular basis of IsK protein regulation by oxidation or chelation.J. Biol. Chem.270199536383641
Crossref | PubMed | ISI | Google Scholar
153 BUSCH G. L., WIESINGER H., GULBINS E., WAGNER H. F., HAMPRECHT B., LANG F.Effect of astroglial cell swelling on pH of acidic intracellular compartments.Biochim. Biophys. Acta12851996212218
Crossref | PubMed | ISI | Google Scholar
154 BUSCH G. L., GÜNTHER E., HEWIG B., ZRENNER E., LANG F.Effect of cell swelling, NH₄Cl and glutamate on acridine orange fluorescence in retinal ganglion cells.Cell. Physiol. Biochem.61996185194
Crossref | ISI | Google Scholar
155 BUSCH G. L., LANG H.-J., LANG F.Studies on the mechanism of swelling-induced lysosomal alkalinization in vascular smooth muscle cells.Pflügers Arch.4311996690696
Crossref | PubMed | ISI | Google Scholar
156 BUSCH G. L., SCHREIBER R., DARTSCH P. C., VÖLKL H., VOM S.DAHL, D. HÄUSSINGER, and F. LANG. Involvement of microtubules in the link between cell volume and pH of acidic cellular compartments in rat and human hepatocytes.Proc. Natl. Acad. Sci. USA91199491659169
Crossref | PubMed | ISI | Google Scholar
157 BUSCH G. L., VÖLKL H., HALLER M., SIEMEN D., MOEST J., KOCH F., LANG F.Vesicular pH is sensitive to changes in cell volume.Cell. Physiol. Biochem.719972534
Crossref | ISI | Google Scholar
158 BUYSE G., DE GREEF C., RAEYMAEKERS L., DROOGMANS G., NILIUS B., EGERMONT J.The ubiquitously expressed pICln protein forms homomeric complexes in vitro.Biochem. Biophys. Res. Commun.2181996822827
Crossref | PubMed | ISI | Google Scholar
159 CABADO A. G., VIEYTES M. R., BOTANA L. M.Effect of ion composition on the changes in membrane potential induced with several stimuli in rat mast cells.J. Cell. Physiol.1581994309316
Crossref | PubMed | ISI | Google Scholar
160 CAHALAN M. D., EHRING G. R., OSIPCHUK Y. V., ROSS P. E.Volume-sensitive Cl⁻ channels in lymphocytes and multidrug-resistant cell lines.Jpn. J. Physiol.44, Suppl. 21994S25S30
PubMed | Google Scholar
161 CALA P. M.Volume regulation by Amphiuma red blood cells: characteristics of volume-sensitive K/H and Na/H exchange.Mol. Physiol.81985199214
Google Scholar
162 CALABRESSE C., VENTURINI L., RONCO G., VILLA P., CHOMIENNE C., BELPOMME D.Butyric acid and its monosaccharide ester induce apoptosis in the HL-60 cell line.Biochem. Biophys. Res. Commun.19519933138
Crossref | PubMed | ISI | Google Scholar
163 CANESSA M., FABRY M. E., BLUMENFELD N., NAGEL R. L.Volume-stimulated, Cl⁻ dependent K⁺ efflux is highly expressed in young human red cells containing normal hemoglobin or HbS.J. Membr. Biol.97198797105
Crossref | PubMed | ISI | Google Scholar
164 CANESSA M., FABRY M. E., NAGEL R. L.Deoxygenation inhibits the volume-stimulated, Cl⁻ dependent K⁺ efflux in SS and young AA cells: a cytosolic Mg²⁺ modulation.Blood70198718611866
PubMed | ISI | Google Scholar
165 CANESSA M., FABRY M. E., SUZUKA S. M., MORGAN K., NAGEL R. L.Na⁺/H⁺ exchange is increased in sickle cell anemia and young normal red cells.J. Membr. Biol.1161990107115
Crossref | PubMed | ISI | Google Scholar
166 CANTIELLO H. F., PRAT A. G., BONVENTRE J. V., CUNNINGHAM C. C., HARTWIG J. H., AUSIELLO D. A.Actin-binding protein contributes to cell volume regulatory ion channel activation in melanoma cells.J. Biol. Chem.268199345964599
Crossref | PubMed | ISI | Google Scholar
167 CAPLAN M. J., STOW J. L., NEWMAN A. P., MADRI J., ANDERSON H. C., FARQUHAR M. G., PALADE G. E., JAMIESON J. D.Dependence on pH of polarized sorting of secreted proteins.Nature3291987632635
Crossref | PubMed | ISI | Google Scholar
168 CARPENTER D. O., FEJTL M., AYRAPETYAN S., SZAROWSKI D. H., TURNER J. N.Dynamic changes in neuronal volume resulting from osmotic and sodium transport manipulations.Acta Biol. Hung.4319923948
PubMed | ISI | Google Scholar
169 CARPENTER J. F., CROWE J. H.Modes of stabilization of a protein by organic solutes during desiccation.Cryobiology251988459470
Crossref | ISI | Google Scholar
170 CARROLL T. P., McINTOSH I., EGAN M. E., ZEITLIN P. L., CUTTING G. R., GUGGINO W. B.Transmembrane mutations alter the channel characteristics of the cystic fibrosis transmembrane conductance regulator expressed in Xenopus oocytes.Cell. Physiol. Biochem.419941018
Crossref | ISI | Google Scholar
171 CARROLL T. P., SCHWIEBERT E. M., GUGGINO W. B.CFTR: structure and function.Cell. Physiol. Biochem.31993388399
Crossref | ISI | Google Scholar
172 CARTER L. C., NICKERSON P. A.Effect of nitrendipine, a calcium antagonist, on cell volume in rat salivary glands after isoproterenol stimulation.Histol. Histopathol.61991339343
PubMed | ISI | Google Scholar
173 CEMERIKIC D., SACKIN H.Substrate activation of mechanosensitive, whole cell currents in renal proximal tubule.Am. J. Physiol.264(Renal Fluid Electrolyte Physiol. 33)1993F697F714
Google Scholar
174 CHACON E., REECE J. M., NIEMINEN A. L., ZAHREBELSKI G., HERMAN B., LEMASTERS J. J.Distribution of electrical potential, pH, free Ca²⁺, and volume inside cultured adult rabbit cardiac myocytes during chemical hypoxia: a multiparameter digitized confocal microscopic study.Biophys. J.661994942952
Crossref | PubMed | ISI | Google Scholar
175 CHAMBERLIN M. E., STRANGE K.Anisosmotic cell volume regulation: a comparative view.Am. J. Physiol.257(Cell Physiol. 26)1989C159C173
Link | Google Scholar
176 CHAN H. C., FU W. O., CHUNG Y. W., HUANG S. J., CHAN P. S. F., WONG P. Y. D.Swelling-induced anion and cation conductances in human epididymal cells.J. Physiol. (Lond.)4781994449460
Crossref | Google Scholar
177 CHAN H. C., NELSON D. J.Chloride-dependent cation conductance activated during cellular shrinkage.Science2571992669671
Crossref | PubMed | ISI | Google Scholar
178 CHAN P. H., FISHMAN R. A.Brain edema: induction in cortical slices by polyunsaturated fatty acids.Science2011978358360
Crossref | PubMed | ISI | Google Scholar
179 CHASE H. S.Jr., and Q. AL-AWQATI. Regulation of the sodium permeability of the luminal border of toad bladder by intracellular sodium and calcium: role of sodium-calcium exchange in the basolateral membrane.J. Gen. Physiol.771981693712
Crossref | PubMed | ISI | Google Scholar
180 CHAUNCEY B., LEITE M. V., GOLDSTEIN L.Renal sorbitol accumulation and associated enzyme activities in diabetes.Enzyme391988231234
Crossref | PubMed | Google Scholar
181 CHEN J. G., KEMPSON S. A.Osmoregulation of neutral amino acid transport.Proc. Soc. Exp. Biol. Med.210199516
Crossref | PubMed | ISI | Google Scholar
182 CHEN J. G., KLUS L. R., STEENBERGEN D. K., KEMPSON S. A.Hypertonic upregulation of amino acid transport system A in vascular smooth muscle cells.Am. J. Physiol.267(Cell Physiol. 36)1994C529C536
Link | Google Scholar
183 CHEN S., INOUE R., INOMATA H., ITO Y.Role of cyclic AMP-induced Cl conductance in aqueous humour formation by the dog ciliary epithelium.Br. J. Pharmacol.112199411371145
Crossref | PubMed | ISI | Google Scholar
184 CHESNEY R. W.Taurine: its biological role and clinical implications.Adv. Pediatr.321985142
PubMed | Google Scholar
185 CHOI D. W.Glutamate neurotoxicity and diseases of the nervous system.Neuron11988623634
Crossref | PubMed | ISI | Google Scholar
186 CHOI D. W., ROTHMAN S. M.The role of glutamate neurotoxicity in hypoxic ischemic neuronal death.Annu. Rev. Neurosci.131990171182
Crossref | PubMed | ISI | Google Scholar
187 CHRISTENSEN O.Mediation of cell volume regulation by Ca²⁺ influx through stretch-activated channels.Nature33019876668
Crossref | PubMed | ISI | Google Scholar
188 CHRISTENSEN O., HOFFMANN E. K.Cell swelling activates K⁺- and Cl⁻-channels as well as nonselective stretch-activated cation channels in Ehrlich ascites tumor cells.J. Membr. Biol.12919921336
Crossref | PubMed | ISI | Google Scholar
189 CHURCH J. G., MILLS G. B., BUICK R. N.Activation of the Na⁺/H⁺ antiport is not required for epidermal growth factor-dependent gene expression, growth inhibition or proliferation in human breast cancer cells.Biochem. J.2571989151157
Crossref | PubMed | ISI | Google Scholar
190 CHURCHWELL K. B., WRIGHT S. H., EMMA F., ROSENBERG P. A., STRANGE K.NMDA receptor activation inhibits neuronal volume regulation after swelling induced by veratridine stimulated Na⁺ influx in rat cortical cultures.J. Neurosci.16199674477457
Crossref | PubMed | ISI | Google Scholar
191 CIVAN M. M., COCA-PRADOS M., PETERSON-YANTORNO K.Pathways signaling the regulatory volume decrease of cultured nonpigmented ciliary epithelial cells.Invest. Ophthalmol. Visual Sci.35199428762886
PubMed | ISI | Google Scholar
192 CLARK, M. E. Non-Donnan effects of organic osmolytes in cell volume changes. In: Current Topics in Membranes and Transport, edited by A. Kleinzeller. New York: Academic, 1987, vol. 30, p. 251–272.
Google Scholar
193 CLARK M. E., HINKE J. A. M., TODD M. E.Studies on water in barnacle muscle fibres. II. Role of ions and organic solutes in swelling of chemically-skinned fibres.J. Exp. Biol.9019814363
ISI | Google Scholar
194 CLEGG J. S.Properties and metabolism of the aqueous cytoplasm and its boundaries.Am. J. Physiol.246(Regulatory Integrative Comp. Physiol. 15)1984R133R151
Google Scholar
195 CLEGG J. S.L-929 cells under hyperosmotic conditions: water, Na⁺, and K⁺.Cell Biophys.131988119132
Crossref | PubMed | Google Scholar
196 CLEGG J. S., JACKSON S. A., FENDL K.Effects of reduced cell volume and water content on glycolysis in L-929 cells.J. Cell. Physiol.1421990386391
Crossref | PubMed | ISI | Google Scholar
197 CLEMENTS R. S., BLUMENTHAL S. A., MORRISON A. D., WINEGRAD A. I.Increased cerebrospinal fluid pressure during treatment of diabetic ketosis.Lancet21971671675
Crossref | PubMed | ISI | Google Scholar
198 CLEMO H. F., BAUMGARTEN C. M.Atrial natriuretic factor decreases cell volume of rabbit atrial and ventricular myocytes.Am. J. Physiol.260(Cell Physiol. 29)1991C681C690
Link | Google Scholar
199 CLEMO H. F., BAUMGARTEN C. M.cGMP and atrial natriuretic factor regulate cell volume of rabbit atrial myocytes.Circ. Res.771995741749
Crossref | PubMed | ISI | Google Scholar
200 CLEMO H. F., BAUMGARTEN C. M.Nitroprusside shrinks cardiac cell volume by inhibiting Na⁺/K⁺/2Cl⁻ cotransport and improves cardiac compliance (Abstract).Circulation841991168
PubMed | ISI | Google Scholar
201 CLEMO H. F., FEHER J. J., BAUMGARTEN C. M.Modulation of rabbit ventricular cell volume and Na⁺/K⁺/2Cl⁻ cotransport by cGMP and atrial natriuretic factor.J. Gen. Physiol.100199289114
Crossref | PubMed | ISI | Google Scholar
202 COATES T. D., WATTS R. G., HARTMAN R., HOWARD T. H.Relationship of F-actin distribution to development of polar shape in human polymorphonuclear neutrophils.J. Cell Biol.1171992765774
Crossref | PubMed | ISI | Google Scholar
203 COELHO-SAMPAIO T., FERREIRA S. T., CASTRO E. J., VIEYRA A.Betaine counteracts urea-induced conformational changes and uncoupling of the human erythrocyte Ca²⁺ pump.Eur. J. Biochem.221199411031110
Crossref | PubMed | Google Scholar
204 COHEN B. J., LECHENE C.Alanine stimulation of passive potassium efflux in hepatocytes is independent of Na⁺-K⁺ pump activity.Am. J. Physiol.258(Cell Physiol. 27)1990C24C29
Link | Google Scholar
205 COHEN D. M., CHIN W. W., GULLANS S. R.Hyperosmotic urea increases transcritption and synthesis of Egr-1 in murine inner medullary collecting duct (mIMCD3) cells.J. Biol. Chem.26919942586525870
PubMed | ISI | Google Scholar
206 COHEN D. M., GULLANS S. R.Urea induces Egr-1 and c-fos expression in renal epithelial cells.Am. J. Physiol.264(Renal Fluid Electrolyte Physiol. 33)1993F593600
Google Scholar
207 COHEN G. M., SUN X. M., SNOWDEN R. T., DINSDALE D., SKILLETER D. N.Key morphological features of apoptosis may occur in the absence of internucleosomal DNA fragmentation.Biochem. J.2861992331334
Crossref | PubMed | ISI | Google Scholar
208 COHEN D. M., WASSERMAN J. C., GULLANS S. R.Immediate early gene and HSP70 expression in hyperosmotic stress in MDCK cells.Am. J. Physiol.261(Cell Physiol. 30)1991C594C601
Link | Google Scholar
209 COLCLASURE G. C., PARKER J. C.Cytosolic protein concentration is the primary volume signal in dog red cells.J. Gen. Physiol.981991881892
Crossref | PubMed | ISI | Google Scholar
210 COLCLASURE G. C., PARKER J. C.Cytosolic protein concentration is the primary volume signal for swelling-induced [K-Cl] cotransport in dog red cells.J. Gen. Physiol.1001992110
Crossref | PubMed | ISI | Google Scholar
211 COLLINS K. D., WASHABAUGH M. W.The Hofmeister effect and the behaviour of water at interfaces.Q. Rev. Biophys.181985323422
Crossref | PubMed | ISI | Google Scholar
212 COLOMBE B. W., MACEY R. I.Effects of calcium on potassium and water transport in human erythrocyte ghosts.Biochim. Biophys. Acta3631974226239
Crossref | PubMed | ISI | Google Scholar
213 COMBES D., YE W. N., ZWICK A., MONSAN P.Effect of salts on enzyme stability.Ann. NY Acad. Sci.5421988710
Crossref | PubMed | Google Scholar
214 CONNOLLY D. L., SHANAHAN C. M., WEISSBERG P. L.Water channels in health and disease.Lancet3471996210212
Crossref | PubMed | ISI | Google Scholar
215 COOPER J. A.The role of actin polymerization in cell motility.Annu. Rev. Physiol.531991585605
Crossref | PubMed | ISI | Google Scholar
216 CORASANTI J. G., GLEESON D., BOYER J. L.Effects of osmotic stresses on isolated rat hepatocytes. I. Ionic mechanisms of cell volume regulation.Am. J. Physiol.258(Gastrointest. Liver Physiol. 21)1990G290G298
Google Scholar
217 CORDER C. N., COLLINS J. G., BRANNAN T. S., SHARMA J.Aldose reductase and sorbitol dehydrogenase distribution in rat kidney.J. Histochem. Cytochem.25197718
Crossref | PubMed | ISI | Google Scholar
218 CORDOBA J., GOTTSTEIN J., BLEI A. T.Glutamine, myo-inositol, and organic brain osmolytes after portacaval anastomosis in the rat: implications for ammonia induced brain edema.Hepatology241996919923
PubMed | ISI | Google Scholar
219 CORNELIUS A. S., REILLY M. P., SUZUKI M., ASAKURA T., HORIUCHI K.The mechanism of chlorpromazine-induced red blood cell swelling.Gen. Pharmacol.251994205210
Crossref | PubMed | Google Scholar
220 CORNET M., DELPIRE E., GILLES R.Relations between cell volume control, microfilaments and microtubule networks in T2 and PC12 cultured cells.J. Physiol. (Paris)8319884349
PubMed | Google Scholar
221 CORNET M., DELPIRE E., GILLES R.Study of microfilaments network during volume regulation process of cultured PC12 cells.Pflügers Arch.4101987223225
Crossref | PubMed | ISI | Google Scholar
222 CORNET M., ISOBE Y., LEMANSKI L. F.Effects of anisosmotic conditions on the cytoskeletal architecture of cultured PC12 cells.J. Morphol.2221994269286
Crossref | PubMed | ISI | Google Scholar
223 CORNET M., LAMBERT I. H., HOFFMANN E. K.Relation between cytoskeleton, hypo-osmotic treatment and volume regulation in Ehrlich ascites tumor cells.J. Membr. Biol.13119935566
Crossref | PubMed | ISI | Google Scholar
224 CORNET M., UBL J., KOLB H. A.Cytoskeleton and ion movements during volume regulation in cultured PC12 cells.J. Membr. Biol.1331993161170
Crossref | PubMed | ISI | Google Scholar
225 COSTA C. J., PIERCE S. K., WARREN M. K.The intracellular mechanism of salinity tolerance in polychaetes: volume regulation by isolated Glycera dibranchiata red coelomocytes.Biol. Bull.1591980626638
Crossref | ISI | Google Scholar
226 COSTA P. M., FERNANDES P. L., FERREIRA H. G., FERREIRA K. T., GIRALDEZ F.Effects of cell volume changes on membrane ionic permeabilities and sodium transport in frog skin (Rana ridibunda).J. Physiol. (Lond.)3931987117
Crossref | Google Scholar
227 COSTA-CASNELLIE M. R., SEGEL G. B., CRAGOE E. J.Jr., and M. A. LICHTMAN. Characterization of the Na⁺/H⁺ exchanger during maturation of HL-60 cells induced by dimethyl sulfoxide.J. Biol. Chem.262198790939097
PubMed | ISI | Google Scholar
228 COSTA-CASNELLIE M. R., SEGEL G. B., LICHTMAN M. A.The Na⁺/H⁺ exchanger in immature and mature granulocytic HL-60 cells.J. Biol. Chem.26319881185111855
PubMed | ISI | Google Scholar
229 COTTON C. U., REUSS L.Effects of changes in mucosal solution Cl⁻ or K⁺ concentration on cell water volume of Necturus gallbladder epithelium.J. Gen. Physiol.971991667686
Crossref | PubMed | ISI | Google Scholar
230 COWLEY B. D., FERRARIS J. D., CARPER D., BURG M. B.In vivo osmoregulation of aldose reductase mRNA, protein, and sorbitol in renal medulla.Am. J. Physiol.258(Renal Fluid Electrolyte Physiol. 27)1990F154F161
Google Scholar
231 CRICHTON E. G., HINTON B. T., PALLONE T. L., HAMMERSTEDT R. H.Hyperosmolality and sperm storage in hibernating bats: prolongation of sperm life by dehydration.Am. J. Physiol.267(Regulatory Integrative Comp. Physiol. 36)1994R1363R1370
Google Scholar
232 CROWE J. H., HOEKSTRA F. A., CROWE L. M.Anhydrobiosis.Annu. Rev. Physiol.541992579599
Crossref | PubMed | ISI | Google Scholar
233 CROWE W. E., ALTAMIRANO J., HUERTO L., ALVAREZ-LEEFMANS F. J.Volume changes in single N1E-115 neuroblastoma cells measured with a fluorescent probe.Neuroscience691995283296
Crossref | PubMed | ISI | Google Scholar
234 CROWE W. E., EHRENFELD J., BROCHIERO E., WILLS N. K.Apical membrane sodium and chloride entry during osmotic swelling of renal (A6) epithelial cells.J. Membr. Biol.14419958191
Crossref | PubMed | ISI | Google Scholar
235 CSERR H. F., DE PASQUALE M., NICHOLSON C., PATLAK C. S., PETTIGREW K. D., RICE M. E.Extracellular volume decreases while cell volume is maintained by ion uptake in rat brain during acute hypernatremia.J. Physiol. (Lond.)4421991277295
Crossref | Google Scholar
236 CSONKA L. N., HANSON A. D.Prokaryotic osmoregulation: genetics and physiology.Annu. Rev. Microbiol.451991569606
Crossref | PubMed | ISI | Google Scholar
237 CUNNINGHAM C. C., STOSSEL T. P., KWIATKOWSKI D. J.Enhanced motility in NIH 3T3 fibroblasts that overexpress gelsolin.Science251199112331236
Crossref | PubMed | ISI | Google Scholar
238 DALL'ASTA V., ROSSI P. A., BUSSOLATI O., GAZZOLA G. C.Regulatory volume decrease of cultured human fibroblasts involves changes in intracellular amino-acid pool.Biochim. Biophys. Acta12201994139145
Crossref | PubMed | ISI | Google Scholar
239 DALL'ASTA V., ROSSI P. A., BUSSOLATI O., GAZZOLA G. C.Response of human fibroblasts to hypertonic stress. Cell shrinkage is counteracted by an enhanced active transport of neutral amino acids.J. Biol. Chem.26919941048510491
PubMed | ISI | Google Scholar
240 DANKER T., GASSNER B., OBERLEITHNER H., SCHWAB A.Extracellular detection of K⁺ release during migration of transformed Madin-Darby canine kidney cells.Pflügers Arch.43319967176
Crossref | PubMed | ISI | Google Scholar
241 DARTSCH P. C., KOLB H. A., BECKMANN M., LANG F.Morphological alterations and cytoskeletal reorganization in opossum kidney (OK) cells during osmotic swelling and volume regulation.Histochemistry10219946975
Crossref | PubMed | Google Scholar
242 DARTSCH P. C., RITTER M., GSCHWENTNER M., LANG H.-J., LANG F.Effects of calcium channel blockers on NIH 3T3 fibroblasts expressing the Ha-ras oncogene.Eur. J. Cell Biol.671995372378
PubMed | ISI | Google Scholar
243 DARTSCH P. C., RITTER M., HÄUSSINGER D., LANG F.Cytoskeletal reorganization in NIH 3T3 fibroblasts expressing the ras oncogene.Eur. J. Cell Biol.631994316325
PubMed | ISI | Google Scholar
244 DASCALU A., NEVO Z., KORENSTEIN R.Hyperosmotic activation of the Na⁺-H⁺ exchanger in a rat bone cell line: temperature dependence and activation pathways.J. Physiol. (Lond.)4561992503518
Crossref | Google Scholar
245 DASGUPTA S., HOHMAN T. C., CARPER D.Hypertonic stress induces alpha B-crystallin expression.Exp. Eye Res.541992461470
Crossref | PubMed | ISI | Google Scholar
246 DAUKAS G., ZIGMOND S. H.Inhibition of receptor-mediated but not fluid-phase endocytosis in polymorphonuclear leukocytes.J. Cell Biol.101198516731679
Crossref | PubMed | ISI | Google Scholar
247 DAUSCH R., SPRING K. R.Regulation of NaCl entry into Necturus gallbladder epithelium by protein kinase C.Am. J. Physiol.266(Cell Physiol. 35)1994C531C535
Link | Google Scholar
248 DAUTRY-VARSAT A., CIECHANOVER A., LODISH H. F.pH and the recycling of transferrin during receptor-mediated endocytosis.Proc. Natl. Acad. Sci. USA80198322582262
Crossref | PubMed | ISI | Google Scholar
249 DAVIS B. A., HOGAN E. M., BORON W. F.Role of G proteins in stimulation of Na-H exchange by cell shrinkage.Am. J. Physiol.262(Cell Physiol. 31)1992C533C536
Link | Google Scholar
250 DAVIS B. A., HOGAN E. M., BORON W. F.Shrinkage-induced activation of Na⁺/H⁺ exchange in barnacle muscle fibers.Am. J. Physiol.266(Cell Physiol. 35)1994C17441753
Link | Google Scholar
251 DAVIS C. W., FINN A. L.Effects of mucosal sodium removal on cell volume in Necturus gallbladder epithelium.Am. J. Physiol.249(Cell Physiol. 18)1985C304C312
Link | Google Scholar
252 DAVIS C. W., FINN A. L.Interactions of sodium transport, cell volume, and calcium in frog urinary bladder.J. Gen. Physiol.891987687702
Crossref | PubMed | ISI | Google Scholar
253 DAY M. L., PICKERING S. J., JOHNSON M. H., COOK D. I.Cell-cycle control of a large-conductance K⁺ channel in mouse early embryos.Nature3651993560562
Crossref | PubMed | ISI | Google Scholar
254 DE CAMILLI P., JAHN R.Pathways to regulated exocytosis in neurons.Annu. Rev. Physiol.521990625645
Crossref | PubMed | ISI | Google Scholar
255 DECKERS C. L. P., LYONS A. B., SAMUEL K., SANDERSON A., MADDY A. H.Alternative pathways of apoptosis induced by methylprednisolone and valinomycin analyzed by flow cytometry.Exp. Cell Res.2081993362370
Crossref | PubMed | ISI | Google Scholar
256 DE GREEF C., SEHRER J., VIANA F., VAN ACKER K., EGGERMONT J., MERTENS L., RAEYMAEKERS L., DROOGMANS G., NILIUS B.Volume-activated chloride currents are not correlated with P-glycoprotein expression.Biochem. J.3071995713718
Crossref | PubMed | ISI | Google Scholar
257 DE GREEF C., VAN DER HEYDEN S., VIANA F., EGGERMONT J., DE BRUIJN E. A., RAEYMAEKERS L., DROOGMANS G., NILIUS B.Lack of correlation between mdr-1 expression and volume activation of chloride currents in rat colon cancer cells.Pflügers Arch.4301995296298
Crossref | PubMed | ISI | Google Scholar
258 DELACUEVA F. I. C., RIGAU T., BONET S., MIRO J., BRIZ M., RODRIGUEZGIL M. B. J. E.Subjecting horse spermatozoa to hypoosmotic incubation: effects of oubain.Theriogenology471997765784
Crossref | PubMed | ISI | Google Scholar
259 DEL BIGIO M. R., FEDOROFF S., QUALTIERE L. F.Morphology of astroglia in colony cultures following transient exposure to potassium ion, hyposmolarity and vasopressin.J. Neurocytol.211992718
Crossref | PubMed | Google Scholar
260 DEL BUFALO D., BUCCI B., D'AGNANO I., ZUPI G.N-methylformamide as a potential therapeutic approach in colon cancer.Dis. Colon Rectum37, Suppl.1994S133S137
Crossref | ISI | Google Scholar
261 DELLASEGA M., GRANTHAM J. J.Regulation of renal tubule cell volume in hypotonic media.Am. J. Physiol.224197312881294
Link | ISI | Google Scholar
262 DELLIPIZZI A. M., McGIFF J. C., ESCALANTE B.Cytochrome P-450 inhibitors attenuate the hypotonic shock-induced increases in K⁺ efflux in LLC-PK₁ cells.Pharmacology501995348356
Crossref | PubMed | ISI | Google Scholar
263 DELPIRE E., CORNET M., GILLES R.Volume regulation in rat pheochromocytoma cultured cells submitted to hyposmotic conditions.Arch. Int. Physiol. Biochim.9919917176
Google Scholar
264 DELPIRE E., GULLANS S. R.Cell volume and K⁺ transport during differentiation of mouse erythroleukemia cells.Am. J. Physiol.266(Cell Physiol. 35)1994C515C523
Link | Google Scholar
265 DELPIRE E., RAUCHMANN M. J., BEIER D. R., HEBERT S. C., GULLANS S. R.Molecular cloning and chromosome localization of a putative basolateral Na⁺-K⁺-2Cl⁻ cotransporter from mouse inner medullary collecting duct (mIMCD-3) cells.J. Biol. Chem.26919942567725683
PubMed | ISI | Google Scholar
266 DEMAUREX N., GRINSTEIN S.Na⁺/H⁺ antiport: modulation by ATP and role in cell volume regulation.J. Exp. Biol.1961994389404
PubMed | ISI | Google Scholar
267 DE MEIS L., INESI G.Effects of organic solvents, methylamines, and urea on the affinity for P_i of the Ca²⁺-ATPase of sarcoplasmic reticulum.J. Biol. Chem.2631988157161
PubMed | ISI | Google Scholar
269 DEMERDASH T. M., SEYREK N., SMOGORZEWSKI M., MARCINKOWSKI W., NASSERMOADELLI S., MASSRY S. G.Pathways through which glucose induces a rise in [Ca²⁺]_i of polymorphonuclear leukocytes of rats.Kidney Int.50199620322040
Crossref | PubMed | ISI | Google Scholar
270 DENKER B. M., SMITH B. L., KUHAJDA F. P., AGRE P.Identification, purification, and partial characterization of a novel M_r 28,000 integral membrane protein from erythrocytes and renal tubules.J. Biol. Chem.26319881563415642
PubMed | ISI | Google Scholar
271 DENOLLE T., PLOUIN P. F.The Na⁺/H⁺ antiport: a target for new antihypertensive agents.Therapie441989215217
PubMed | ISI | Google Scholar
272 DERMIETZEL R., HWANG T.-K., BUETTNER R., HOFER A., DOTZLER E., KREMER M., DEUTZMANN R., THINNES F. P., FISHMAN G. I., SPRAY D. C., SIEMEN D.Cloning and in situ localization of a brain derived porin that constitutes a large conductance anion channel in astrocytic plasma membranes.Proc. Natl. Acad. Sci. USA911994499503
Crossref | PubMed | ISI | Google Scholar
272a DE SMET P., SIMAELS J., VAN DRIESSCHE W.Regulatory volume decrease in a renal distal tubular cell line (A6). I. Role of K⁺ and Cl⁻.Pflügers Arch.4301995936944
Crossref | PubMed | ISI | Google Scholar
273 DEUTSCH C., CHEN L. Q.Heterologous expression of specific K⁺ channels in T lymphocytes: functional consequences for volume regulation.Proc. Natl. Acad. Sci. USA9019931003610040
Crossref | PubMed | ISI | Google Scholar
274 DEVIN A., GUERIN B., RIGOULET M.Dependence of flux size and efficiency of oxidative phosphorylation on external osmolarity in isolated rat liver: role of adenine nucleotide carrier.Biochim. Biophys. Acta12719961320
Crossref | ISI | Google Scholar
275 DEW L. A., OWEN R. G.Jr., and M. J. MULROY. Changes in size and shape of auditory hair cells in vivo during noise induced temporary threshold shift.Hear. Res.66199399107
Crossref | PubMed | ISI | Google Scholar
276 DIENER M.Segmental differences along the crypt axis in the response of cell volume to secretagogues or hypotonic medium in the rat colon.Pflügers Arch.4261994462464
Crossref | PubMed | ISI | Google Scholar
277 DIENER M., GARTMANN V.Effect of somatostatin on cell volume, Cl⁻ currents, and transepithelial Cl⁻ transport in rat distal colon.Am. J. Physiol.266(Gastrointest. Liver Physiol. 29)1994G1043G1052
Google Scholar
278 DIENER M., HELMLE-KOLB C., MURER H., SCHARRER E.Effect of short-chain fatty acids on cell volume and intracellular pH in rat distal colon.Pflügers Arch.4241993216223
Crossref | PubMed | ISI | Google Scholar
279 DIENER M., NOBLES M., RUMMEL W.Activation of basolateral Cl⁻ channels in the rat colonic epithelium during regulatory volume decrease.Pflügers Arch.4211992530538
Crossref | PubMed | ISI | Google Scholar
280 DIENER M., PETER A., SCHARRER E.The role of volume-sensitive Cl⁻ channels in the stimulation of chloride absorption by short-chain fatty acids in the rat colon.Acta Physiol. Scand.1511994385394
Crossref | PubMed | Google Scholar
281 DIENER M., SCHARRER E.The leukotriene D₄ receptor blocker, SK&F 104353, inhibits volume regulation in isolated crypts from the rat distal colon.Eur. J. Pharmacol.2381993217222
Crossref | PubMed | ISI | Google Scholar
282 DIENER M., SCHARRER E.The effect of short-chain fatty acids on Cl⁻ and K⁺ conductance in rat colonic crypts.Pflügers Arch.4261994472480
Crossref | PubMed | ISI | Google Scholar
283 DING G., FRANKI N., CONDEELIS J., HAYS R. M.Vasopressin depolymerizes F-actin in toad bladder epithelial cells.Am. J. Physiol.260(Cell Physiol. 29)1991C9C16
Link | Google Scholar
284 DINGLEY A. J., KING N. J., KING G. F.An NMR investigation of the changes in plasma membrane triglyceride and phospholipid precursors during the activation of T-lymphocytes.Biochemistry31199290989106
Crossref | PubMed | ISI | Google Scholar
285 DINGLEY A. J., VEALE M. F., KING N. J., KING G. F.Two-dimensional ¹H NMR studies of membrane changes during the activation of primary T lymphocytes.Immunomethods41994127138
Crossref | PubMed | Google Scholar
286 DONG J. M., LIM L.Selective up regulation of alpha 1 chimaerin mRNA in SK N SH neuroblastoma by K⁺ induced depolarisation.Eur. J. Biochem.2361996820826
Crossref | PubMed | Google Scholar
287 DOROSHENKO P., NEHER E.Volume-sensitive chloride conductance in bovine chromaffin cell membrane.J. Physiol. (Lond.)4491992197218
Crossref | Google Scholar
288 DORUP I., CLAUSEN T.Characterization of bumetanide sensitive Na⁺ and K⁺ transport in rat skeletal muscle.Acta Physiol. Scand.1581996119127
Crossref | PubMed | Google Scholar
289 DOWNEY G. P., GRINSTEIN S., SUE A.-A-QUAN, B. CZABAN, and C. K. CHAN. Volume regulation in leukocytes: requirement for an intact cytoskeleton.J. Cell. Physiol.163199596104
Crossref | PubMed | ISI | Google Scholar
289a DREWS, G., G. ZEMPEL, P. KRIPPEIT-DREWS, S. BRITSCH, G. L. BUSCH, N. K. KABA, and F. LANG. Ion channels involved in insulin release are activated by osmotic swelling of pancreatic β-cells. Biochim. Biophys. Acta. In press.
Google Scholar
290 DUBE L., PARENT L., SAUVE R.Hypotonic shock activates a maxi K⁺ channel in primary cultured proximal tubule cells.Am. J. Physiol.259(Renal Fluid Electrolyte Physiol. 28)1990F348F356
Google Scholar
291 DUHM J., GÖBEL B. O.Na⁺-K⁺ transport and volume of rat erythrocytes under dietary K⁺ deficiency.Am. J. Physiol.246(Cell Physiol. 15)1984C20C29
Link | Google Scholar
292 DUMAN J. G., WU D. W., XU L., TURSMAN D., OLSEN T. M.Adaptations of insects to subzero temperatures.Q. Rev. Biol.661991387410
Crossref | ISI | Google Scholar
293 DUNHAM P. B.Effects of urea on K-Cl cotransport in LK sheep red blood cells: evidence for two signals of swelling.Am. J. Physiol.268(Cell Physiol. 37)1995C1026C1032
Link | Google Scholar
294 DUNHAM P. B., JESSEN F., HOFFMANN E. K.Inhibition of Na-K-Cl cotransport in Ehrlich ascites cells by antiserum against purified proteins of the cotransporter.Proc. Natl. Acad. Sci. USA87199068286832
Crossref | PubMed | ISI | Google Scholar
295 DUNHAM P. B., KLIMCZAK J., LOGUE P. J.Swelling activation of K-Cl cotransport in LK sheep erythrocytes: a three state process.J. Gen. Physiol.1011993733766
Crossref | PubMed | ISI | Google Scholar
296 DUNN F. W., ROUX M. H., FARHADIAN F., SABRI K., OSSART C., SAMUEL J. L., RAPPAPORT L., HAMON G.HR 720, a novel angiotensin receptor antagonist inhibits the angiotensin II induced trophic effects, fibronectin release and fibronectin EIIIA(+) expression in rat aortic vascular smooth muscle cells in vitro.J. Pharmacol. Exp. Ther.2801997447453
PubMed | ISI | Google Scholar
297 EATON W. A., HOFRICHTER J.Hemoglobin S gelation and sickle cell disease.Blood70198712451266
Crossref | PubMed | ISI | Google Scholar
298 EATON W. A., HOFRICHTER J., ROSS P. D.Editorial: delay time of gelation: a possible determinant of clinical severity in sickle cell disease.Blood471976621627
PubMed | ISI | Google Scholar
299 ECHEVARRIA M., VERKMAN A. S.Optical measurement of osmotic water transport in cultured cells. Role of glucose transporters.J. Gen. Physiol.991992573589
Crossref | PubMed | ISI | Google Scholar
300 ECHEVARRIA M., WINDHAGER E. E., TATE S. S., FRINDT G.Cloning and expression of AQP3, a water channel from the medullary collecting duct of rat kidney.Proc. Natl. Acad. Sci. USA9119941099711001
Crossref | PubMed | ISI | Google Scholar
301 EDELMAN J. L., SACHS G., ADORANTE J. S.Ion transport asymmetry and functional coupling in bovine pigmented and nonpigmented ciliary epithelial cells.Am. J. Physiol.266(Cell Physiol. 35)1994C1210C1221
Link | Google Scholar
302 EDMANDS S. D., HUGHS K. S., LEE S. Y., MEYER S. D., SAARI E., YANCEY P. H.Time-dependent aspects of osmolyte changes in rat kidney, urine, blood and lens with sorbinil and galactose feeding.Kidney Int.481995344353
Crossref | PubMed | ISI | Google Scholar
303 EDMANDS S., YANCEY P. H.Effects on rat renal osmolytes of extended treatment with an aldose reductase inhibitor.Comp. Biochem. Physiol. C Pharmacol. Toxicol. Endocrinol.1031992499502
Crossref | ISI | Google Scholar
304 EDMONDS B., GIBB A. J., COLQUHOUN D.Mechanisms of activation of muscle nicotinic acetylcholine receptors and the time course of endplate currents.Annu. Rev. Physiol.571995469493
Crossref | PubMed | ISI | Google Scholar
305 ELLIOT S. J., SCHILLING W. P.Oxidant stress alters Na⁺ pump and Na⁺-K⁺-Cl⁻ cotransporter activities in vascular endothelial cells.Am. J. Physiol.263(Heart Circ. Physiol. 32)1992H96H102
Google Scholar
306 ELWYN D. H., BRYAN-BROWN C. W., SHOEMAKER W. C.Nutritional aspects of body water dislocations in postoperative and depleted patients.Ann. Surg.18219757685
Crossref | PubMed | ISI | Google Scholar
307 ENGSTRÖM K. G., OHLSSON L.Acute and long-term biphasic volume alterations in rat type-II somatotrophs during GH secretory stimulation.Biochim. Biophys. Acta11351992318322
Crossref | PubMed | ISI | Google Scholar
308 ENGSTRÖM K. G., SANDSTRÖM P.-E., SEHLIN J.Volume regulation in mouse pancreatic beta-cells is mediated by a furosemide-sensitive mechanism.Biochim. Biophys. Acta10911991145150
Crossref | PubMed | ISI | Google Scholar
309 EPSTEIN, W. Osmoregulation by potassium transport in Escherichia coli. FEMS Microbiol. Rev. 39: 73–78, 1986.
Google Scholar
310 ERIKSSON L. E. G., BEVING H.Calcium- and lead-activated morphological changes in human erythrocytes: a spin label study of the cytoplasm.Arch. Biochem. Biophys.3031993296301
Crossref | PubMed | ISI | Google Scholar
311 ERZURUM S. C., KUS M. L., BOHSE C., ELSON E. L., WORTHEN G. S.Mechanical properties of HL60 cells: role of stimulation and differentiation in retention in capillary sized pores.Am. J. Respir. Cell. Mol. Biol.51991230241
Crossref | PubMed | ISI | Google Scholar
312 FAFF-MICHALAK L., REICHENBACH A., DETTMER D., KELLNER K., ALBRECHT J.K⁺-, hypoosmolarity-, and NH⁺₄-induced taurine release from cultured rabbit Müller cells: role of Na⁺ and Cl⁻ ions and relation to cell volume changes.Glia101994114120
Crossref | PubMed | ISI | Google Scholar
313 FALKE L. C., MISLER S.Activity of ion channels during volume regulation by clonal N1E115 neuroblastoma cells.Proc. Natl. Acad. Sci. USA86198939193923
Crossref | PubMed | ISI | Google Scholar
314 FEIG P. U., D'OCCHIO M. A., BOYLAN J. W.Lymphocyte membrane sodium-proton exchange in spontaneously hypertensive rats.Hypertension91987282288
Crossref | PubMed | ISI | Google Scholar
315 FELDMAN G. M., ZIYADEH F. N., MILLS J. W., BOOZ G. W., KLEINZELLER A.Proprionate induces cell swelling and K⁺ accumulation in shark rectal gland.Am. J. Physiol.257(Cell Physiol. 26)1989C377C384
Link | Google Scholar
316 FELIPE A., SNYDERS D. J., DEAL K. K., TAMKUN M. M.Influence of cloned voltage-gated K⁺ channel expression on alanine transport, Rb⁺ uptake, and cell volume.Am. J. Physiol.265(Cell Physiol. 34)1993C1230C1238
Link | Google Scholar
317 FELTES T. F., SEIDEL C. L., DENNISON D. K., AMICK S., ALLEN J. C.Relationship between functional Na⁺ pumps and mitogenesis in cultured coronary artery smooth muscle cells.Am. J. Physiol.264(Cell Physiol. 33)1993C169C178
Link | Google Scholar
318 FERNANDES P. R., DEWEY M. J.Genetic control of erythrocyte volume regulation: effect of a single gene (rol) on cation metabolism.Am. J. Physiol.267(Cell Physiol. 36)1994C211C219
Link | Google Scholar
319 FERRARIS J. D., BURG M. B., WILLIAMS C. K., PETERS E. M., GARCIA-PEREZ A.Betaine transporter cDNA cloning and effect of osmolytes on its mRNA induction.Am. J. Physiol.270(Cell Physiol. 39)1996C650C654
Link | Google Scholar
320 FERRARIS J. D., WILLIAMS C. K., JUNG K. Y., BEDFORD J. J., BURG M. B., GARCIA-PEREZ A.ORE, a eukaryotic minimal essential osmotic response element. The aldose reductase gene in hyperosmotic stress.J. Biol. Chem.27119961831818321
Crossref | PubMed | ISI | Google Scholar
321 FERRARIS J. D., WILLIAMS C. K., MARTIN B. M., BURG M. B., GARCIA-PEREZ A.Cloning, genomic organization, and osmotic response of the aldose reductase gene.Proc. Natl. Acad. Sci. USA9119941074210746
Crossref | PubMed | ISI | Google Scholar
322 FERRER-MARTINEZ A., CASADO F. J., FELIPE A., PASTORANGLADA M.Regulation of Na⁺, K⁺ ATPase and the Na⁺/K⁺/Cl cotransporter in the renal epithelial cell line NBL 1 under osmotic stress.Biochem. J.3191996337342
Crossref | PubMed | ISI | Google Scholar
323 FIEVET B., GUIZOUARN H., PELLISSIER B., GARCIA F.ROMEU, and R. MOTAIS. Evidence for a K⁺-H⁺ exchange in trout red blood cells.J. Physiol. (Lond.)4621993597607
Crossref | Google Scholar
324 FIEVET B., GABILLAT N., BORGESE F., MOTAIS R.Expression of band 3 anion exchanger induces chloride current and taurine transport: structure-function analysis.EMBO J.14199551585169
Crossref | PubMed | ISI | Google Scholar
325 FINBERG L.Hypernatremic (hypertonic) dehydration in infants.N. Engl. J. Med.2891973196198
Crossref | PubMed | ISI | Google Scholar
326 FINEGOLD D., LATTIMER S. A., NOLLE S., BERNSTEIN M., GREENE D. A.Polyol pathway activity and myo-inositol metabolism: a suggested relationship in the pathogenesis of diabetic neuropathy.Diabetes321983988992
Crossref | PubMed | ISI | Google Scholar
327 FINK K., ZENTNER J., GOTHERT M.Increased GABA release in the human brain cortex as a potential pathogenetic basis of hyperosmolar diabetic coma.J. Neurochem.62199414761481
Crossref | PubMed | ISI | Google Scholar
328 FINKENZELLER G., NEWSOME W., LANG F., HÄUSSINGER D.Increase of c-jun mRNA upon hypoosmotic cell swelling of rat hepatoma cells.FEBS Lett.3401994163166
Crossref | PubMed | ISI | Google Scholar
329 FINN A. L., REUSS L.Effects of changes in the composition of the serosal solution on the electrical properties of the toad urinary bladder epithelium.J. Physiol. (Lond.)2501975541558
Crossref | Google Scholar
330 FISCHER H., ILLEK B., NEGULESCU P. A., CLAUSS W., MACHEN T. E.Carbachol-activated calcium entry into HT-29 cells is regulated by both membrane potential and cell volume.Proc. Natl. Acad. Sci. USA89199214381442
Crossref | PubMed | ISI | Google Scholar
331 FISHER R. S., SPRING K. R.Intracellular activities during volume regulation by Necturus gallbladder.J. Membr. Biol.781984187199
Crossref | PubMed | ISI | Google Scholar
332 FLATMAN P. W.The effects of magnesium on potassium transport in ferret red cells.J. Physiol. (Lond.)3971988471487
Crossref | Google Scholar
333 FLIEGEL L., FRÖHLICH O.The Na⁺/H⁺ exchanger: an update on structure, regulation, and cardiac physiology.Biochem. J.2961993273285
Crossref | PubMed | ISI | Google Scholar
334 FLOCK S., LABARBE R., HOUSSIER C.Osmotic effectors and DNA structure: effect of glycine on precipitation of DNA by multivalent cations.J. Biomol. Struct. Dyn.13199587102
Crossref | PubMed | ISI | Google Scholar
335 FLOUR M. P., RONOT X., VINCENT F., BENOIT B., ADOLPHE M.Differential temperature sensitivity of cultured cells from cartilaginous or bone origin.Biol. Cell.7519928387
Crossref | PubMed | ISI | Google Scholar
336 FLOWERS T. J., TROKE P. F., YEO A. R.The mechanism of salt tolerance in halophytes.Annu. Rev. Plant Physiol.28197789121
Crossref | Google Scholar
337 FONDACARO J. D.Intestinal ion transport and diarrheal disease.Am. J. Physiol.250(Gastrointest. Liver Physiol. 13)1986G1G8
Google Scholar
338 FOSKETT J. K.[Ca²⁺]_i modulation of Cl⁻ content controls cell volume in single salivary acinar cells during fluid secretion.Am. J. Physiol.259(Cell Physiol. 28)1990C998C1004
Link | Google Scholar
339 FOSKETT J. K., MELVIN J. E.Activation of salivary secretion: coupling of cell volume and [Ca²⁺]_i in single cells.Science244198915821585
Crossref | PubMed | ISI | Google Scholar
340 FOSKETT J. K., SPRING K. R.Involvement of calcium and cytoskeleton in gallbladder epithelial cell volume regulation.Am. J. Physiol.248(Cell Physiol. 17)1985C27C36
Link | Google Scholar
341 FOSKETT J. K., WONG M. M., SUE G.A QUAN, and M. A. ROBERTSON. Isosmotic modulation of cell volume and intracellular ion activities during stimulation of single exocrine cells.J. Exp. Zool.2681994104110
Crossref | PubMed | Google Scholar
342 FOSSE M., BERG T. O., O'REILLY D. S., SEGLEN P. O.Vanadate inhibition of hepatocytic autophagy. Calcium-modulated and osmolality-modulated antagonism by asparagine.Eur. J. Biochem.23019951724
Crossref | PubMed | Google Scholar
343 FRANCO R. S., PALASCAK M., THOMPSON H., RUCKNAGEL D. L., JOINER C. H.Dehydration of transferrin receptor positive sickle reticulocytes during continuous or cyclic deoxygenation: role of KCl cotransport and extracellular calcium.Blood88199643594365
PubMed | ISI | Google Scholar
344 FRASER C. L., SWANSON R. A.Female sex hormones inhibit volume regulation in rat brain astrocyte culture.Am. J. Physiol.267(Cell Physiol. 36)1994C909C914
Link | Google Scholar
345 FREDERIKSEN O., LEYSSAC P. P., SKINNER S. L.Sensitive osmometer function of juxtaglomerular cells in vitro.J. Physiol. (Lond.)2521975669679
Crossref | Google Scholar
346 FREEMAN C. J., BOOKCHIN R. M., ORTIZ O. E., LEW V. L.K-permeabilized human red cells lose an alkaline, hypertonic fluid containing excess K⁺ over diffusible anions.J. Membr. Biol.961987235241
Crossref | PubMed | ISI | Google Scholar
347 FRIEDMAN J. E., HADDAD G. G.Major differences in [Ca²⁺]_i response to anoxia between neonatal and adult rat CA1 neurons: role of [Ca²⁺]_o and [Na⁺]_o .J. Neurosci.1319936372
Crossref | PubMed | ISI | Google Scholar
348 FRIEDMAN S. M.The relation of cell volume, cell sodium and the transmembrane sodium gradient to blood pressure.J. Hypertens.819906773
Crossref | PubMed | ISI | Google Scholar
349 FRIGERI A., GROPPER M. A., UMENISHI F., KAWASHIMA M., BROWN D., VERKMAN A. S.Localization of MIWC and GLIP water channel homologs in neuromuscular, epithelial and glandular tissues.J. Cell Sci.108199529933002
PubMed | ISI | Google Scholar
350 FRIZZELL R. A., RECHKEMMER G., SHOEMAKER R. L.Altered regulation of airway epithelial cell chloride channels in cystic fibrosis.Science2331986558560
Crossref | PubMed | ISI | Google Scholar
351 FU W. J., KUWAHARA M., CRAGOE E. J.Jr., and F. MARUMO. Mechanisms of regulatory volume increase in collecting duct cells.Jpn. J. Physiol.431993745757
Crossref | PubMed | Google Scholar
352 FUJITA Y., IWASA Y., NODA Y.The effect of polyhydric alcohols on the thermal denaturation of lysozyme as measured by differential scanning calorimetry.Bull. Chem. Soc. Jpn.55198218961900
Crossref | ISI | Google Scholar
353 FULTON, A. B. How crowded is the cytoplasm? Cell 30: 345–347, 1982.
Google Scholar
354 FURLONG T. J., MORIYAMA T., SPRING K. R.Activation of osmolyte efflux from cultured renal papillary epithelial cells.J. Membr. Biol.1231991269277
Crossref | PubMed | ISI | Google Scholar
355 FURLONG T. J., SPRING K. R.Mechanisms underlying volume regulatory decrease by Necturus gallbladder epithelium.Am. J. Physiol.258(Cell Physiol. 27)1990C1016C1024
Link | Google Scholar
356 FUSHIMI K., UCHIDA S., HARA Y., HIRATA Y., MARUMO F., SASAKI S.Cloning and expression of apical membrane water channel of rat kidney collecting tubule.Nature3611993549552
Crossref | PubMed | ISI | Google Scholar
357 FUSHIMI K., VERKMAN A. S.Low viscosity in the aqueous domain of cell cytoplasm measured by picosecond polarization microfluorimetry.J. Cell Biol.1121991719725
Crossref | PubMed | ISI | Google Scholar
358 GABBAY K. H., O'SULLIVAN J. B.The sorbitol pathway. Enzyme localization and content in normal and diabetic nerve and cord.Diabetes171968239243
Crossref | PubMed | ISI | Google Scholar
359 GAGNON J., OUIMET D., NGUYEN H., LAPRADE R., LE GRIMELLEC C., CARRIÉRE S., CARDINAL J.Cell volume regulation in the proximal convoluted tubule.Am. J. Physiol.243(Renal Fluid Electrolyte Physiol. 12)1982F408F415
Google Scholar
360 GALCHEVA-GARGOVA Z., DERIJARD B., WU I. H., DAVIS R. J.An osmosensing signal transduction pathway in mammalian cells.Science2651994806808
Crossref | PubMed | ISI | Google Scholar
361 GALIETTA L. J. V., RASOLA A., RUGOLO M., ZOTTINI M., MASTROCOLA T., GRUENERT D. C., ROMEO G.Extracellular 2-chloroadenosine and ATP stimulate volume-sensitive Cl⁻ current and calcium mobilization in human tracheal 9HTEo- cells.FEBS Lett.30419926165
Crossref | PubMed | ISI | Google Scholar
362 GALIETTA L. J. V., ROMEO G., ZEGARRAMORAN O.Volume regulatory taurine release in human tracheal 9HTEo and multidrug resistant 9HTEo/Dx cells.Am. J. Physiol.271(Cell Physiol. 40)1996C728C735
Link | Google Scholar
363 GALKIN A. A., KHODOROV B. I.The involvement of furosemide-sensitive ion counter transport system in the autoregulation of macrophage volume: role of cytoskeleton.Biol. Membr.51988302307
ISI | Google Scholar
364 GAMBA G., MIYANOSHITA A., LOMBARDI M., LYTTON J., LEE W.-S., HEDIGER M. A., HEBERT S. C.Molecular cloning, primary structure and characterization of two members of the mammalian electroneutral sodium-(potassium)-chloride cotransporter family expressed in kidney.J. Biol. Chem.26919941771317722
PubMed | ISI | Google Scholar
365 GAMBA G., SALTZBERG S. N., LOMBARDI M., MIYANOSHITA A., LYTTON J., HEDIGER M. A., BRENNER B. M., HEBERT S. C.Primary structure and functional expression of a cDNA encoding the thiazide-sensitive, electroneutral sodium chloride cotransporter.Proc. Natl. Acad. Sci. USA90199327492753
Crossref | PubMed | ISI | Google Scholar
366 GAO D. Y., LIU J., LIU C., McGANN L. E., WATSON P. F., KLEINHANS F. W., MAZUR P., CRITSER E. S., CRITSER J. K.Prevention of osmotic injury to human spermatozoa during addition and removal of glycerol.Hum. Reprod.10199511091122
Crossref | PubMed | ISI | Google Scholar
367 GAO Y., VANHOUTTE P. M.Hypotonic solutions induce epithelium-dependent relaxation of isolated canine bronchi.Lung1701992339347
Crossref | PubMed | ISI | Google Scholar
368 GARCIA-PEREZ A.Organic osmolytes in the kidney.Semin. Nephrol.131993182190
PubMed | ISI | Google Scholar
369 GARCIA-PEREZ A., BURG M. B.Importance of organic osmolytes for osmoregulation by renal medullary cells.Hypertension161990595602
Crossref | PubMed | ISI | Google Scholar
370 GARCIA-PEREZ A., BURG M. B.Renal medullary organic osmolytes.Physiol. Rev.71199110811115
Link | ISI | Google Scholar
371 GARCIA-PEREZ A., BURG M. B.Role of organic osmolytes in adaptation of renal cells to high osmolality.J. Membr. Biol.1191991113
Crossref | PubMed | ISI | Google Scholar
372 GARCIA-PEREZ, A., and J. D. FERRARIS. Aldose reductase gene expression and osmoregulation in mammalian renal cells. In: Cellular and Molecular Physiology of Cell Volume Regulation, edited by K. Strange. Boca Raton, FL: CRC, 1994, p. 373–382.
Google Scholar
373 GARCIA-PEREZ A., MARTIN B., MURPHY H. R., UCHIDA S., MURER H., COWLEY B. D., HANDLER J. S., BURG M. B.Molecular cloning of cDNA coding for kidney aldose reductase: regulation of specific mRNA accumulation by NaCl-mediated osmotic stress.J. Biol. Chem.26419891681516821
PubMed | ISI | Google Scholar
374 GARCIA-ROMEU F., BORGESE F., GUIZOUARN H., FIEVET B., MOTAIS R.A role for the anion exchanger AE1 (band 3 protein) in cell volume regulation.Cell. Mol. Biol.421996985994
PubMed | ISI | Google Scholar
375 GARLAND A., JORDAN J. E., NECHELES J., ALGER L. E., SCULLY M. M., MILLER R. J., RAY D. W., WHITE S. R., SOLWAY J.Hypertonicity, but not hypothermia, elicits substance P release from rat c fiber neurons in primary culture.J. Clin. Invest.95199523592366
Crossref | PubMed | ISI | Google Scholar
376 GARNER M. M., BURG M. B.Macromolecular crowding and confinement in cells exposed to hypertonicity.Am. J. Physiol.266(Cell Physiol. 35)1994C877C892
Link | Google Scholar
377 GARTY H., FURLONG T. J., ELLIS D. E., SPRING K. R.Sorbitol permease: an apical membrane transporter in cultured renal papillary epithelial cells.Am. J. Physiol.260(Renal Fluid Electrolyte Physiol. 29)1991F650F656
Google Scholar
378 GARVIN J. L., SPRING K. R.Regulation of apical membrane ion transport in Necturus gallbladder.Am. J. Physiol.263(Cell Physiol. 32)1992C187C193
Link | Google Scholar
379 GAUSSIN V., BAQUET A., HUE L.Cell shrinkage follows, rather than mediates, the short-term effects of glucagon on carbohydrate metabolism.Biochem. J.28719921720
Crossref | PubMed | ISI | Google Scholar
380 GAZZOLA G. C., DALL'ASTA V., NUCCI F. A., ROSSI P. A., BUSSOLATI O., HOFFMANN E. K., GUIDOTTI G. G.Role of amino acid transport system A in the control of cell volume in cultured human fibroblasts.Cell. Physiol. Biochem.11991131142
Crossref | Google Scholar
381 GECK P., PFEIFFER B.Na⁺K⁺2Cl⁻ cotransport in animal cells: its role in volume regulation.Ann. NY Acad. Sci.4561985166182
Crossref | PubMed | ISI | Google Scholar
382 GEIGER B.Membrane-cytoskeleton interaction.Biochim. Biophys. Acta7371983305341
Crossref | PubMed | ISI | Google Scholar
383 GEKKO K., MORIKAWA T.Thermodynamics of polyol-induced thermal stabilization of chymotrypsinogen.J. Biochem.9019815160
Crossref | PubMed | ISI | Google Scholar
384 GERLSMA S. Y.Reversible denaturation of ribonuclease in aqueous solutions as influenced by polyhydric alcohols and some other additives.J. Biol. Chem.2431968957961
PubMed | ISI | Google Scholar
385 GHANAYEM B. I., SULLIVAN C. A.Assessment of the haemolytic activity of 2-butoxyethanol and its major metabolite, butoxyacetic acid, in various mammals including humans.Hum. Exp. Toxicol.121993305311
Crossref | PubMed | ISI | Google Scholar
386 GIBSON J. S., HALL A. C.Stimulation of the KCl co-transport in equine erythrocytes by hydrostatic pressure: effects of kinase/phosphatase inhibition.Pflügers Arch.4291995446448
Crossref | PubMed | ISI | Google Scholar
387 GILLES R.Comparative aspects of cell osmoregulation and volume control.Renal Physiol. Biochem.111988277288
PubMed | Google Scholar
388 GILLES R.Volume regulation in cells of euryhaline invertebrates.Curr. Top. Membr. Transp.301987205248
Crossref | ISI | Google Scholar
389 GILLES, R., and M. GILLES-BALLIEN. Transport Processes, Iono- and Osmoregulation. Heidelberg, Germany: Springer-Verlag, 1985, p. 483.
Google Scholar
390 GILLES, R., A. KLEINZELLER, and L. BOLIS. Cell volume control: fundamental and comparative aspects in animal care. In: Current Topics in Membranes and Transport, edited by A. Kleinzeller. New York: Academic, 1987, vol. 30.
Google Scholar
391 GILLES R., PEQUEUX A.Cell volume regulation in crustaceans: relationship between mechanisms for controlling the osmolarity of extracellular and intracellular fluids.J. Exp. Zool.2151981351362
Crossref | Google Scholar
392 GILLIN A. G., SANDS J. M.Characteristics of osmolarity-stimulated urea transport in rat IMCD.Am. J. Physiol.262(Renal Fluid Electrolyte Physiol. 31)1992F1061F1067
Google Scholar
393 GILLIN A. G., STAR R. A., SANDS J. M.Osmolarity-stimulated urea transport in rat terminal IMCD: role of intracellular calcium.Am. J. Physiol.265(Renal Fluid Electrolyte Physiol. 34)1993F272F277
Google Scholar
394 GILMORE J. A., McGANN L. E., LIU J., GAO D. Y., PETER A. T., KLEINHANS F. W., CRITSER J. K.The effect of cryoprotectant solutes on water permeability of human spermatozoa.Biol. Reprod.531995985995
Crossref | PubMed | ISI | Google Scholar
395 GINZBURG M.Dunaliella: a green alga adapted to salt.Adv. Bot. Res.14198793185
Crossref | ISI | Google Scholar
396 GIOVANNELLI L., SHIROMANI P. J., JIRIKOWSKI G. F., BLOOM F. E.Expression of c-Fos protein by immunohistochemically identified oxytocin neurons in the rat hypothalamus upon osmotic stimulation.Brain Res.58819924148
Crossref | PubMed | ISI | Google Scholar
397 GLEESON D., CORASANTI J. G., BOYER J. L.Effects of osmotic stresses on isolated rat hepatocytes. II. Modulation of intracellular pH.Am. J. Physiol.258(Gastrointest. Liver Physiol. 21)1990G299G307
Google Scholar
398 GODT R. E., FOGACA R. T., ANDREWS M. A., NOSEK T. M.Influence of ionic strength on contractile force and energy consumption of skinned fibers from mammalian and crustacean striated muscle.Adv. Exp. Med. Biol.3321993763774
Crossref | PubMed | Google Scholar
399 GOLDSTEIN L.Organic solute profiles and transport in the rat renal medulla.Am. J. Kidney Dis.141989310312
Crossref | PubMed | ISI | Google Scholar
400 GOLDSTEIN L., KLEINZELLER A.Cell volume regulation in lower vertebrates.Curr. Top. Membr. Transp.301987181204
Crossref | ISI | Google Scholar
401 GOLLNICK F., MEYER R., STOCKEM W.Visualization and measurement of calcium transients in Amoeba proteus by fura-2 fluorescence.Eur. J. Cell Biol.551991262271
PubMed | ISI | Google Scholar
402 GORODESKI G. I., DE SANTIS B. J., GOLDFARB J., UTIAN W. H., HOPFER U.Osmolar changes regulate the paracellular permeability of cultured human cervical epithelium.Am. J. Physiol.269(Cell Physiol. 38)1995C870C877
Link | Google Scholar
403 GOSLING M., POYNER D. R., SMITH J. W.Effects of arachidonic acid upon the volume sensitive chloride current in rat osteoblast like (ROS 17/2.8) cells.J. Physiol. (Lond.)4931996613623
Crossref | Google Scholar
404 GOSS G. G., WOODSIDE M., WAKABAYASHI S., POUYSSEGUR J., WADDELL T., DOWNEY G. P., GRINSTEIN S.ATP dependence of NHE-1, the ubiquitous isoform of the Na⁺/H⁺ antiporter. Analysis of phosphorylation and subcellular localization.J. Biol. Chem.269199487418748
PubMed | ISI | Google Scholar
405 GOTTLIEB R. A., NORDBERG J., SKOWRONSKI E., BABIOR B. M.Apoptosis induced in Jurkat cells by several agents is preceded by intracellular acidification.Proc. Natl. Acad. Sci. USA931996654658
Crossref | PubMed | ISI | Google Scholar
406 GRAF J., HADDAD P., HÄUSSINGER D., LANG F.Cell volume regulation in liver.Renal Physiol. Biochem.111988202220
PubMed | Google Scholar
407 GRANITZER M., MOUNTIAN I., DE SMET P., VAN DRIESSCHE W.Effect of ouabain on membrane conductances and volume in A6 cells.Renal. Physiol. Biochem.171994223231
PubMed | Google Scholar
408 GRANT A., BURCHELL A.GTP and ATP increase the transport capacity of the T1 transport protein of the microsomal glucose-6-phosphatase complex.Biochem. Soc. Trans.18199012511252
Crossref | PubMed | ISI | Google Scholar
409 GRANT A., TOSH D., BURCHELL A.Liver perfusion with hyper-osmotic media stimulates microsomal glucose-6-phosphatase activity (Abstract).Biochem. Soc. Trans.21199339S
Crossref | PubMed | Google Scholar
410 GREEN R. B., SLATTERY M. J., GIANFERRARI E., KIZER N. L., McCOY D. E., STANTON B. A.Hyperosmolality inhibits sodium absorption and cloride secretion in mIMCD K2 cells.Am. J. Physiol.271(Renal Fluid Electrolyte Physiol. r0)1996F1248F1254
Google Scholar
411 GREENE D. A., LATTIMER S. A., SIMA A. A.Sorbitol, phosphoinositides and sodium-potassium-ATPase in the pathogenesis of diabetic complications.N. Engl. J. Med.3161987599606
Crossref | PubMed | ISI | Google Scholar
412 GREENWALD J. E., APKON M., HRUSKA K. A., NEEDLEMAN P.Stretch-induced atriopeptin secretion in the isolated rat myocyte and its negative modulation by calcium.J. Clin. Invest.83198910611065
Crossref | PubMed | ISI | Google Scholar
413 GREENWAY H., OSMOND C. B.Salt responses of enzymes from species differing in salt tolerance.Plant Physiol.491972256259
Crossref | PubMed | ISI | Google Scholar
414 GREER M. A., GREER S. E., MARUTA S.Hyposmolar stimulation of secretion of thyrotropin, prolactin, and luteinizing hormone does not require extracellular calcium and is not inhibited by colchicine, cytochalasin B, ouabain, or tetrodotoxin.Proc. Soc. Exp. Biol. Med.1931990203209
Crossref | PubMed | ISI | Google Scholar
415 GREER M. A., GREER S. E., OPSAHL Z., McCAFFERTY L., MARUTA S.Hyposmolar stimulation of in vitro pituitary secretion of luteinizing hormone: a potential clue to the secretory process.Endocrinology113198315311533
Crossref | PubMed | ISI | Google Scholar
416 GREGER R.Ion transport mechanisms in thick ascending limb of Henle's loop of mammalian nephron.Physiol. Rev.651985760797
Link | ISI | Google Scholar
417 GREGER R., ALLERT N., FRÖBE U., NORMANN C.Increase in cytosolic Ca²⁺ regulates exocytosis and Cl⁻ conductance in HT29 cells.Pflügers Arch.4241993329334
Crossref | PubMed | ISI | Google Scholar
418 GRINSTEIN S., CLARKE C. A., DUPRÉ A., ROTHSTEIN A.Volume-induced increase of anion permeability in human lymphocytes.J. Gen. Physiol.801982801823
Crossref | PubMed | ISI | Google Scholar
419 GRINSTEIN S., CLARKE C. A., ROTHSTEIN A.Increased anion permeability during volume regulation in human lymphocytes.Philos. Trans. R. Soc. Lond. B Biol. Sci.2991982509518
Crossref | PubMed | ISI | Google Scholar
420 GRINSTEIN S., CLARKE C. A., ROTHSTEIN A.Activation of Na⁺/H⁺ exchange in lymphocytes by osmotically induced volume changes and by cytoplasmic acidification.J. Gen. Physiol.821983619638
Crossref | PubMed | ISI | Google Scholar
421 GRINSTEIN S., CLARKE C. A., ROTHSTEIN A., GELFAND E. W.Volume-induced anion conductance in human B lymphocytes is cation independent.Am. J. Physiol.245(Cell Physiol. 14)1983C160C163
Link | Google Scholar
422 GRINSTEIN, S., S. COHEN, J. D. GOETZ, A. ROTHSTEIN, A. MELLORS, and E. W. GELFAND. Activation of the Na⁺-H⁺ antiport by changes in cell volume and by phorbol esters: possible role of protein kinase. In: Current Topics in Membranes and Transport. New York: Academic, 1986, vol. 26, p. 115–134.
Google Scholar
423 GRINSTEIN S., COHEN S., SARKADI B., ROTHSTEIN A.Induction of ⁸⁶Rb fluxes by Ca²⁺ and volume changes in thymocytes and their isolated membranes.J. Cell. Physiol.1161983352362
Crossref | PubMed | ISI | Google Scholar
424 GRINSTEIN S., DUPRÉ A., ROTHSTEIN A.Volume regulation by human lymphocytes. Role of calcium.J. Gen. Physiol.791982849868
Crossref | PubMed | ISI | Google Scholar
425 GRINSTEIN S., FOSKETT J. K.Ionic mechanisms of cell volume regulation in leukocytes.Annu. Rev. Physiol.521990399414
Crossref | PubMed | ISI | Google Scholar
426 GRINSTEIN S., GOETZ-SMITH J. D., STEWART D., BERESFORD B. J., MELLORS A.Protein phosphorylation during activation of Na⁺/H⁺ exchange by phorbol esters and by osmotic shrinking. Possible relation to cell pH and volume regulation.J. Biol. Chem.261198680098016
PubMed | ISI | Google Scholar
427 GRINSTEIN S., MACK E., MILLS G. B.Osmotic activation of the Na⁺/H⁺ antiport in protein kinase C-depleted lymphocytes.Biochem. Biophys. Res. Commun.1341986813
Crossref | PubMed | ISI | Google Scholar
428 GRINSTEIN S., ROTIN D., MASON M. J.Na⁺/H⁺ exchange and growth factor induced cystolic pH changes. Role in cellular proliferation.Biochim. Biophys. Acta98819897397
Crossref | PubMed | ISI | Google Scholar
429 GRINSTEIN S., SMITH J. D.Calcium-independent cell volume regulation in human lymphocytes. Inhibition by charybdotoxin.J. Gen. Physiol.95199097120
Crossref | PubMed | ISI | Google Scholar
430 GRINSTEIN S., WOODSIDE M., SARDET C., POUYSSÉGUR J., ROTIN D.Activation of the Na⁺/H⁺ antiporter during cell volume regulation. Evidence for a phosphorylation-independent mechanism.J. Biol. Chem.26719922382323828
PubMed | ISI | Google Scholar
431 GRINSTEIN S., WOODSIDE M., WADDELL T. K., DOWNEY G. P., ORLOWSKI J., POUYSSÉGUR J., WONG D. C. P., FOSKETT J. K.Focal localization of the NHE-1 isoform of the Na⁺/H⁺ antiport: assessment of effects on intracellular pH.EMBO J.12199352095218
Crossref | PubMed | ISI | Google Scholar
432 GROENEVELD A. B., VAN-LAMBALGEN A. A., VAN-DEN-BOS G. C., NAUTA J. J., THIJS L. G.Metabolic vasodilatation with glucose-insulin-potassium does not change the heterogeneous distribution of coronary blood flow in the dog.Cardiovasc. Res.261992757764
Crossref | PubMed | ISI | Google Scholar
433 GROSSMAN E. B., HEBERT S. C.Renal inner medullary choline dehydrogenase activity: characterization and modulation.Am. J. Physiol.256(Renal Fluid Electrolyte Physiol. 25)1989F107F112
Google Scholar
434 GROSSO A., MEDA P., DE SOUSA R. C.Effects of anions and/or cell volume on the permeance of an apical water pathway induced by Hg in toad skin epithelium.J. Membr. Biol.13419934152
Crossref | PubMed | ISI | Google Scholar
435 GRÜNDER S., THIEMANN A., PUSCH M., JENTSCH T. J.Regions involved in the opening of the CIC-2 chloride channel by voltage and cell volume.Nature3601992759762
Crossref | PubMed | ISI | Google Scholar
436 GRUNEWALD J. M., GRUNEWALD R. W., KINNE R. K. H.Ion content and cell volume in isolated collecting duct cells: effect of hypotonicity.Kidney Int.441993509517
Crossref | PubMed | ISI | Google Scholar
437 GRUNEWALD J. M., GRUNEWALD R. W., KINNE R. K. H.Regulation of ion content and cell volume in isolated rat renal IMCD cells under hypertonic conditions.Am. J. Physiol.267(Renal Fluid Electrolyte Physiol. 36)1994F13F19
Google Scholar
438 GSCHWENTNER M., JUNGWIRTH A., HOFER S., WÖLL E., RITTER M., SUSANNA A., SCHMARDA A., REIBNEGGER G., PINGGERA G. M., LEITINGER M., FRICK J., DEETJEN P., PAULMICHL M.Blockade of swelling-induced chloride channels by phenol derivatives.Br. J. Pharmacol.11819964148
Crossref | PubMed | ISI | Google Scholar
439 GSCHWENTNER M., NAGL U. O., SCHMARDA A., WÖLL E., RITTER M., WAITZ W., DEETJEN P., PAULMICHL M.Structure-function relation of a cloned epithelial chloride channel.Renal Physiol. Biochem.171994148152
PubMed | Google Scholar
440 GSCHWENTNER M., NAGL U. O., WÖLL E., SCHMARDA A., RITTER M., PAULMICHL M.Antisense oligonucleotides suppress cell-volume-induced activation of chloride channels.Pflügers Arch.4301995464470
Crossref | PubMed | ISI | Google Scholar
441 GSCHWENTNER M., SUSANNA A., WÖLL E., RITTER M., NAGL U. O., SCHMARDA A., LAICH A., PINGGERA G. M., ELLEMUNTER H., HUEMER H., DEETJEN P., PAULMICHL M.Antiviral drugs from the nucleoside analog family block volume-activated chloride channels.Mol. Med.11995407417
Crossref | PubMed | ISI | Google Scholar
442 GUDER W. G., BECK F. X., SCHMOLKE M.Regulation and localization of organic osmolytes in mammalian kidney.Klin. Wochenschr.68199010911095
Crossref | PubMed | Google Scholar
443 GUGGINO W. B.Functional heterogeneity in the early distal tubule of the Amphiuma kidney: evidence for two modes of Cl⁻ and K⁺ transport across the basolateral cell membrane.Am. J. Physiol.250(Renal Fluid Electrolyte Physiol. 19)1986F430F440
Google Scholar
444 GUGGINO W. B., OBERLEITHNER H., GIEBISCH G.Relationship between cell volume and ion transport in the early distal tubule of the Amphiuma kidney.J. Gen. Physiol.8619853158
Crossref | PubMed | ISI | Google Scholar
445 GUHARAY F., SACHS F.Stretch-activated single ion channel currents in tissue-cultured embryonic chick skeletal muscle.J. Physiol. (Lond.)3521984685701
Crossref | Google Scholar
446 GULBINS E., BISSONNETTE R., MAHBOUBI A., MARTIN S., NISHIOKA W., BRUNNER T., BAIER G., BAIER-BITTERLICH G., BYRD C., LANG F., KOLESNICK R., ALTMAN A., GREEN D.Fas-induced apoptosis is mediated via a ceramide-initiated RAS signaling pathway.Immunity21995341351
Crossref | PubMed | ISI | Google Scholar
447 GULBINS E., BRENNER B., SCHLOTTMANN K., WELSCH J., HEINLE H., KOPPENHÖFER U., LINDERKAMP O., COGGESHALL K. M., LANG F.Fas-induced programmed cell death is mediated by a ras-regulated O₂-synthesis.Immunology891996205212
Crossref | PubMed | ISI | Google Scholar
448 GULBINS E., COGGESHALL K. M., BRENNER B., SCHLOTTMANN K., LINDERKAMP O., LANG F.Fas-induced apoptosis is mediated by activation of a ras and rac-protein regulated signaling pathway.J. Biol. Chem.27119962638926394
Crossref | PubMed | ISI | Google Scholar
449 GULBINS E., SZABO I., BALTZER K., LANG F.Ceramide induced inhibition of T-lymphocyte voltage gated potassium channel is mediated by tyrosine kinases.Proc. Natl. Acad. Sci USA94199776617666
Crossref | PubMed | ISI | Google Scholar
450 GULBINS E., SZABO I., LANG F.Physiology of Fas-induced programmed cell death.Cell. Physiol. Biochem.61996361375
Crossref | ISI | Google Scholar
451 GULBINS E., WELSCH J., LEPPLE-WIENHUES A., HEINLE H., LANG F.Inhibition of Fas-induced apoptotic cell death by osmotic cell shrinkage.Biochem. Biophys. Res. Commun.2361997517521
Crossref | PubMed | ISI | Google Scholar
452 GULLANS S. R., BLUMENFELD J. D., BALSCHI J. A., KALETA M., BRENNER R. M., HEILIG C. W., HEBERT S. C.Accumulation of major organic osmolytes in renal inner medulla in dehydration.Am. J. Physiol.255(Renal Fluid Electrolyte Physiol. 24)1988F626F634
Google Scholar
453 GULLANS S. R., VERBALIS J. G.Control of brain volume during hyperosmolar and hypoosmolar conditions.Annu. Rev. Med.441993289301
Crossref | PubMed | ISI | Google Scholar
454 GUPTA S., SHIMIZU M., OHIRA K., VAYUVEGULA B.T cell activation via the T cell receptor: a comparison between WT31 (defining alpha/beta TcR)-induced and anti-CD3-induced activation of human T lymphocytes.Cell. Immunol.13219912644
Crossref | PubMed | ISI | Google Scholar
455 GUSTAFSON L. A., JUMELLELACLAU M. N., VAN WOERKOM G. M., VAN KUILENBURG A. B. P., MEIJER A. J.Cell swelling and glycogen metabolism in hepatocytes from fasted rats.Biochim. Biophys. Acta13181997184190
Crossref | PubMed | ISI | Google Scholar
456 GUSTAFSON L. A., ROMP N., VAN WOERKOM G. M., MEIJER A. J.Carbamoyl phosphate and ureagenesis are not involved in amino-acid-stimulated glycogenesis.Eur. J. Biochem.2231994553556
Crossref | PubMed | Google Scholar
457 GUZMAN M., VELASCO G., CASTRO J., ZAMMIT V. A.Inhibition of carnitine palmitoyltransferase I by hepatocyte swelling.FEBS Lett.3441994239241
Crossref | PubMed | ISI | Google Scholar
458 HAAS A. L.Ubiquitin-mediated processes in erythroid cell maturation.Adv. Exp. Med. Biol.3071991191205
Crossref | PubMed | Google Scholar
459 HAAS M., McMANUS T. J.Effect of norepinephrine on swelling-induced potassium transport in duck red cells. Evidence against a volume-regulatory decrease under physiological conditions.J. Gen. Physiol.851985649667
Crossref | PubMed | ISI | Google Scholar
460 HABERICH F. J., AZIZ O., NOWACKI P. E.Über einen osmoreceptorisch tätigen Mechanismus in der Leber.Pflügers Arch.28519657389
Crossref | ISI | Google Scholar
461 HACKENTHAL E., TAUGNER R.Hormonal signals and intracellular messengers for renin secretion.Mol. Cell. Endocrinol.471986112
Crossref | PubMed | ISI | Google Scholar
462 HAGMANN J., DAGAN D., BURGER M. M.Release of endosomal content induced by plasma membrane tension: video image intensification time lapse analysis.Exp. Cell Res.1981992298304
Crossref | PubMed | ISI | Google Scholar
463 HAHN K., DE BIASIO R., TAYLOR D. L.Patterns of elevated free calcium and calmodulin activation in living cells.Nature3591992736738
Crossref | PubMed | ISI | Google Scholar
464 HAINSWORTH A. H., HENDERSON R. M., HICKMAN M. E., HLADKY S. B., ROWLANDS T., TWENTYMAN P. R., BARRAND M. A.Hypotonicity-induced anion fluxes in cells expressing the multidrug-resistance-associated protein, MRP.Pflügers Arch.4321996234240
Crossref | PubMed | ISI | Google Scholar
465 HALESTRAP A. P.Regulation of mitochondrial metabolism through changes in matrix volume.Biochem. Soc. Trans.221994522529
Crossref | PubMed | ISI | Google Scholar
466 HALESTRAP A. P.The regulation of the matrix volume of mammalian mitochondria in vivo and in vitro and its role in the control of mitochondrial metabolism.Biochim. Biophys. Acta9731989355382
Crossref | PubMed | ISI | Google Scholar
467 HALESTRAP A. P., DAVIDSON A. M., POTTER W. D.Mechanisms involved in the hormonal regulation of mitochondrial function through changes in the matrix volume.Biochim. Biophys. Acta10181990278281
Crossref | ISI | Google Scholar
468 HALL S. K., ZHANG J. P., LIEBERMAN M.Cyclic AMP prevents activation of a swelling-induced chloride-sensitive conductance in chick heart cells.J. Physiol. (Lond.)4881995359369
Crossref | Google Scholar
469 HALLBRUCKER C., LANG F., GEROK W., HÄUSSINGER D.Cell swelling increases bile flow and taurocholate excretion into bile in isolated perfused rat liver.Biochem. J.2811992593595
Crossref | PubMed | ISI | Google Scholar
470 HALLBRUCKER C., RITTER M., LANG F., GEROK W., HÄUSSINGER D.Hydroperoxide metabolism in rat liver. K⁺ channel activation, cell volume changes and eicosanoid formation.Eur. J. Biochem.2111993449458
Crossref | PubMed | Google Scholar
471 HALLBRUCKER C., VOM S.DAHL, F. LANG, and D. HÄUSSINGER. Control of hepatic proteolysis by amino acids. The role of cell volume.Eur. J. Biochem.1971991717724
Crossref | PubMed | Google Scholar
472 HALLBRUCKER C., VOM S.DAHL, F. LANG, W. GEROK, and D. HÄUSSINGER. Inhibition of hepatic proteolysis by insulin. Role of hormone-induced alterations of the cellular K⁺ balance.Eur. J. Biochem.1991991467474
Crossref | PubMed | Google Scholar
473 HALLBRUCKER C., VOM S.DAHL, F. LANG, W. GEROK, and D. HÄUSSINGER. Modification of liver cell volume by insulin and glucagon.Pflügers Arch.4181991519521
Crossref | PubMed | ISI | Google Scholar
474 HALLBRUCKER C., VOM S.DAHL, M. RITTER, F. LANG, and D. HÄUSSINGER. Effects of urea on K⁺ fluxes and cell volume in perfused rat liver.Pflügers Arch.4281994552560
Crossref | PubMed | ISI | Google Scholar
475 HALLOWS K. R., FRANK R. S.Changes in mechanical properties with DMSO-induced differentiation of HL-60 cells.Biorheology291992295309
Crossref | PubMed | ISI | Google Scholar
476 HALLOWS K. R., KNAUF P. A.Regulatory volume decrease in HL-60 cells: importance of rapid changes in permeability of Cl⁻ and organic solutes.Am. J. Physiol.267(Cell Physiol. 36)1994C1045C1056
Link | Google Scholar
477 HALLOWS K. R., LAW F. Y., PACKMAN C. H., KNAUF P. A.Changes in cytoskeletal actin content, F-actin distribution, and surface morphology during HL-60 cell volume regulation.J. Cell. Physiol.16719966071
Crossref | PubMed | ISI | Google Scholar
478 HALLOWS K. R., PACKMAN C. H., KNAUF P. A.Acute cell volume changes in anisotonic media affect F-actin content of HL-60 cells.Am. J. Physiol.261(Cell Physiol. 30)1991C1154C1161
Link | Google Scholar
479 HALLOWS K. R., RESTREPO D., KNAUF P. A.Control of intracellular pH during regulatory volume decrease in HL-60 cells.Am. J. Physiol.267(Cell Physiol. 36)1994C1057C1066
Link | Google Scholar
480 HAMMERMAN M. R., SACKTOR B., DAUGHADAY W. H.Myo-inositol transport in renal brush border vesicles and its inhibition by d-glucose.Am. J. Physiol.239(Renal Fluid Electrolyte Physiol. 8)1980F113F120
Google Scholar
481 HAMPTON M. B., CHAMBERS S. T., VISSERS M. C., WINTERBOURN C. C.Bacterial killing by neutrophils in hypertonic environments.J. Infect. Dis.1691994839846
Crossref | PubMed | ISI | Google Scholar
482 HAN J., LEE J. D., BIBBS L., ULEVITCH R. J.A MAP kinase targeted by endotoxin and hyperosmolarity in mammalian cells.Science2651994808811
Crossref | PubMed | ISI | Google Scholar
483 HAND S. C., SOMERO G. N.Urea and methylamine effects on rabbit muscle phosphofructokinase catalytic stability and aggregation state as a function of pH and temperature.J. Biol. Chem.2571982734741
PubMed | ISI | Google Scholar
484 HANDLER J. S., KWON H. M.Regulation of renal cell organic osmolyte transport by tonicity.Am. J. Physiol.265(Cell Physiol. 34)1993C1449C1455
Link | Google Scholar
485 HANSEN S. H., SANDVIG K., VAN DEURS B.Clathrin and HA2 adaptors: effects of potassium depletion, hypertonic medium, and cytosol acidification.J. Cell Biol.12119936172
Crossref | PubMed | ISI | Google Scholar
486 HANSSON E.Metabotropic glutamate receptor activation induces astroglial swelling.J. Biol. Chem.26919942195521961
PubMed | ISI | Google Scholar
487 HANSSON E., JOHANSSON B. B., WESTERGREN I., RONNBACK L.Mechanisms of glutamate induced swelling in astroglial cells.Acta Neurochir. Suppl. Wien.6019941214
PubMed | Google Scholar
488 HANSSON E., RONNBACK L.Receptor-mediated volume regulation in astrocytes in primary culture.Neuropharmacology3119928587
Crossref | PubMed | ISI | Google Scholar
489 HARBAK H., SIMONSEN L. O.The K⁺ channels activated during regulatory volume decrease (RVD) are distinct from those activated by Ca²⁺-mobilizing agonists in Ehrlich mouse ascites tumor cells. (Abstract).J. Physiol. (Lond.)482199512P
Google Scholar
490 HARDY S. P., GOODFELLOW H. R., VALVERDE M. A., GILL D. R., SEPULVEDA V., HIGGINS C. F.Protein kinase C-mediated phosphorylation of the human multidrug resistance P-glycoprotein regulates cell volume-activated chloride channels.EMBO J.1419956875
Crossref | PubMed | ISI | Google Scholar
491 HART R. A., GILTINAN D. M., LESTER P. M., REIFSNYDER H., OGEZ J. R., BUILDER S. E.Effect of environment on insulin-like growth factor I refolding selectivity.Biotechnol. Appl. Biochem.201994217232
PubMed | ISI | Google Scholar
492 HARTWIG J. H.Mechanisms of actin rearrangements mediating platelet activation.J. Cell Biol.118199214211442
Crossref | PubMed | ISI | Google Scholar
493 HARVEY B. J.Cross-talk and epithelial ion transport.Curr. Opin. Nephrol. Hypertens.31994523528
Crossref | PubMed | Google Scholar
494 HASEGAWA H., MA T., SKACH W., MATTHAY M. A., VERKMAN A. S.Molecular cloning of a mercurial-insensitive water channel expressed in selected water-transporting tissues.J. Biol. Chem.269199454975500
Crossref | PubMed | ISI | Google Scholar
495 HÄUSSINGER D.The role of cellular hydration for the regulation of cell function.Biochem. J.3131996697710
Crossref | PubMed | ISI | Google Scholar
496 HÄUSSINGER D., GEROK W., LANG F.Cell volume and hepatic metabolism.Adv. Comp. Environ. Physiol.1419933365
Crossref | Google Scholar
497 HÄUSSINGER D., HALLBRUCKER C., SAHA N., LANG F., GEROK W.Cell volume and bile acid excretion.Biochem. J.2881992681689
Crossref | PubMed | ISI | Google Scholar
498 HÄUSSINGER D., HALLBRUCKER C., VOM S.DAHL, S. DECKER, U. SCHWEIZER, F. LANG, and W. GEROK. Cell volume is a major determinant of proteolysis control in liver.FEBS Lett.28319917072
Crossref | PubMed | ISI | Google Scholar
499 HÄUSSINGER D., HALLBRUCKER C., VOM S.DAHL, F. LANG, and W. GEROK. Cell swelling inhibits proteolysis in perfused rat liver.Biochem. J.2721990239242
Crossref | PubMed | ISI | Google Scholar
500 HÄUSSINGER D., LANG F.Exposure of perfused liver to hypotonic conditions modifies cellular nitrogen metabolism.J. Cell. Biochem.431990355361
Crossref | PubMed | ISI | Google Scholar
501 HÄUSSINGER D., LANG F.Cell volume and hormone action.Trends Pharmacol. Sci.131992371373
Crossref | PubMed | ISI | Google Scholar
502 HÄUSSINGER D., LANG F., BAUERS K., GEROK W.Interactions between glutamine metabolism and cell-volume regulation in perfused rat liver.Eur. J. Biochem.1881990689695
Crossref | PubMed | Google Scholar
503 HÄUSSINGER D., LANG F., BAUERS K., GEROK W.Control of hepatic nitrogen metabolism and glutathione release by cell volume regulatory mechanisms.Eur. J. Biochem.1931990891898
Crossref | PubMed | Google Scholar
504 HÄUSSINGER D., LANG F., GEROK W.Regulation of cell function by the cellular hydration state.Am. J. Physiol.267(Endocrinol. Metab. 30)1994E343E355
Google Scholar
505 HÄUSSINGER D., LAUBENBERGER J., VOM S.DAHL, T. ERNST, S. BAYER, M. LANGER, W. GEROK, and J. HENNIG. Proton magnetic resonance spectroscopy studies on human brain myo-inositol in hypo-osmolarity and hepatic encephalopathy.Gastroenterology107199414751480
Crossref | PubMed | ISI | Google Scholar
506 HÄUSSINGER D., NEWSOME W., VON DAHL S., STOLL B., NOE B., SCHREIBER R., WETTSTEIN M., LANG F.Control of liver cell function by the hydration state.Biochem. Soc. Trans.221994497502
Crossref | PubMed | ISI | Google Scholar
507 HÄUSSINGER D., ROTH E., LANG F., GEROK W.Cellular hydration state: an important determinant of protein catabolism in health and disease.Lancet341199313301332
Crossref | PubMed | ISI | Google Scholar
508 HÄUSSINGER D., SAHA N., HALLBRUCKER C., LANG F., GEROK W.Involvement of microtubules in the swelling-induced stimulation of transcellular taurocholate transport in perfused rat liver.Biochem. J.2911993355360
Crossref | PubMed | ISI | Google Scholar
509 HÄUSSINGER D., STEHLE T., LANG F.Volume regulation in liver: further characterization by inhibitors and ionic substitutions.Hepatology111990243254
Crossref | PubMed | ISI | Google Scholar
510 HÄUSSINGER D., STOLL B., MORIMOTO Y., LANG F., GEROK W.Anisoosmotic liver perfusion: redox shifts and modulation of alpha-ketoisocaproate and glycine metabolism.Biol. Chem. Hoppe-Seyler3731992723734
Crossref | PubMed | ISI | Google Scholar
511 HÄUSSINGER D., STOLL B., VOM S.DAHL, P. A. THEODOROPOULOS, E. MARKOGIANNAKIS, A. GRAVANIS, F. LANG, and C. STOURNARAS. Effect of hepatocyte swelling on microtubule stability and tubulin mRNA levels.Biochem. Cell. Biol.7219941219
Crossref | PubMed | ISI | Google Scholar
512 HAWKINS R. A., JESSY J., MANS A. M., DE JOSEPH M. R.Effect of reducing brain glutamine synthesis on metabolic symptoms of hepatic encephalopathy.J. Neurochem.60199310001006
Crossref | PubMed | ISI | Google Scholar
513 HAYAMA N., WANG W., ROBINSON T. V., KRAMER R. E., SCHNEIDER E. G.Osmolality and potassium cause alterations in the volume of glomerulosa cells.Endocrinology132199312301234
Crossref | PubMed | ISI | Google Scholar
514 HAYAMA N., WANG W., SCHNEIDER E. G.Osmolality-induced changes in aldosterone secretion involve a chloride-dependent process.Am. J. Physiol.268(Regulatory Integrative Comp. Physiol. 37)1995R8R13
Google Scholar
515 HAYES M. R., McGIVAN J. D.Differential effects of starvation on alanine and glutamine transport in isolated rat hepatocytes.Biochem. J.2041982365368
Crossref | PubMed | ISI | Google Scholar
516 HAZAMA A., OKADA Y.Biphasic rises in cytosolic free Ca²⁺ in association with activation of K⁺ and Cl⁻ conductance during the regulatory volume decrease in cultured human epithelial cells.Pflügers Arch.4161990710714
Crossref | PubMed | ISI | Google Scholar
517 HAZAMA A., OKADA Y.Ca²⁺ sensitivity of volume-regulatory K⁺ and Cl⁻ channels in cultured human epithelial cells.J. Physiol. (Lond.)4021988687702
Crossref | Google Scholar
518 HAZAMA A., OKADA Y.Involvement of Ca²⁺-induced Ca²⁺ release in the volume regulation of human epithelial cells exposed to a hypotonic medium.Biochem. Biophys. Res. Commun.1671990287293
Crossref | PubMed | ISI | Google Scholar
519 HEBERT S. C.Hypertonic cell volume regulation in mouse thick limbs. I. ADH dependency and nephron heterogeneity.Am. J. Physiol.250(Cell Physiol. 19)1986C907C919
Link | Google Scholar
520 HEBERT S. C.Hypertonic cell volume regulation in mouse thick limbs. II. Na⁺/H⁺ and Cl⁻/HCO⁻₃ exchange in basolateral membranes.Am. J. Physiol.250(Cell Physiol. 19)1986C920C931
Link | Google Scholar
521 HEBERT S. C., ANDREOLI T. E.Effects of antidiuretic hormone on cellular conductive pathways in mouse medullary thick ascending limbs of Henle. II. Determinants of the ADH-mediated increases in transepithelial voltage and in net Cl⁻ absorption.J. Membr. Biol.801984221233
Crossref | PubMed | ISI | Google Scholar
522 HEBERT S. C., SUN A. M.Hypotonic cell volume regulation in mouse medullary thick ascending limb: effects of ADH.Am. J. Physiol.255(Renal Fluid Electrolyte Physiol. 24)1988F962F969
Google Scholar
523 HEDIGER M. A., KANAI Y.Expression cloning and characterization of the glutamate transporter in neurons.Renal Physiol. Biochem.171994161164
PubMed | Google Scholar
524 HEILIG C. W., STROMSKI M. E., BLUMENFELD J. D., LEE J. P., GULLANS S. R.Characterization of the major brain osmolytes that accumulate in salt-loaded rats.Am. J. Physiol.257(Renal Fluid Electrolyte Physiol. 26)1989F1108F1116
Google Scholar
525 HEILIG C. W., STROMSKI M. E., GULLANS S. R.Methylamine and polyol responses to salt loading in renal inner medulla.Am. J. Physiol.257(Renal Fluid Electrolyte Physiol. 26)1989F1117F1123
Google Scholar
526 HENDERSON L. M., CHAPPELL J. B., JONES O. T.Superoxide generation is inhibited by phospholipase A₂ inhibitors. Role for phospholipase A₂ in the activation of the NADPH oxidase.Biochem. J.2641989249255
Crossref | PubMed | ISI | Google Scholar
527 HENSON J. H., SCHATTEN G.Calcium regulation of the actin-mediated cytoskeletal transformation of sea urchin coelomocytes.Cell. Motil.31983525534
Crossref | PubMed | Google Scholar
528 HERMANSSON K., SPRING K. R.Potassium induced changes in cell volume of gallbladder epithelium.Pflügers Arch.407, Suppl.1986S90S99
Crossref | ISI | Google Scholar
529 HESKETH J. E., PRYME I. F.Interaction between mRNA, ribosomes and the cytoskeleton.Biochem. J.2771991110
Crossref | PubMed | ISI | Google Scholar
530 HEUSER J. E.Effects of cytoplasmic acidification on clathrin lattice morphology.J. Cell Biol.1081989401411
Crossref | PubMed | ISI | Google Scholar
531 HEUSER J. E., ANDERSON R. G. W.Hypertonic media inhibit receptor-mediated endocytosis by blocking clathrin-coated pit formation.J. Cell Biol.1081989389400
Crossref | PubMed | ISI | Google Scholar
532 HIGGINS C. F.Volume-activated chloride currents associated with the multidrug resistance P-glycoprotein.J. Physiol. (Lond.)482, Suppl.199531S36S
Crossref | Google Scholar
533 HIGGINS, C. F., J. CAIRNEY, D. A. STIRLING, L. SUTHERLAND, and I. R. BOOTH. Osmotic regulation of gene expression: ionic strength as an intracellular signal? Trends Biochem. Sci. 12: 339–344, 1987.
Google Scholar
534 HIGGINS J., HODGES N. A., OLLIFF C. J., PHILLIPS A. J.A comparative investigation of glycinebetaine and dimethyl sulfoxide as liposome cryoprotectants.J. Pharm. Pharmacol.391987577582
Crossref | PubMed | ISI | Google Scholar
535 HILAL-DANDAN R., BRUNTON L. L.Transmembrane mechanochemical coupling in cardiac myocytes: novel activation of G_i by hyposmotic swelling.Am. J. Physiol.269(Heart Circ. Physiol. 38)1995H798H804
Google Scholar
536 HILL A. E.Osmotic flow in membrane pores of molecular size.J. Membr. Biol.1371994197203
Crossref | PubMed | ISI | Google Scholar
537 HJELLE J. T., HO A. K., MILLER-HJELLE M. A., REITH M., STEIDLEY K. R., DUFFIELD R., BUTLER T., DOBBIE J. W.Multiple drug classes and hyperosmolarity alter binding of muscarinic drugs to mesothelial cells in vitro.Adv. Perit. Dial.11199536
PubMed | Google Scholar
538 HOCHMAN D. W., BARABAN S. C., OWENS J. W., SCHWARTZKROIN P. A.Dissociation of synchronization and excitability in furosemide blockade of epileptiform activity.Science270199599102
Crossref | PubMed | ISI | Google Scholar
539 HOFFMANN E. K., DUNHAM P. B.Membrane mechanisms and intracellular signalling in cell volume regulation.Int. Rev. Cytol.1611995173262
Crossref | PubMed | Google Scholar
540 HOFFMANN E. K., HENDIL K. B.The role of amino acids and taurine in isosmotic intracellular regulation in Ehrlich ascites mouse tumour cells.J. Comp. Physiol.1081976279286
Crossref | ISI | Google Scholar
541 HOFFMANN E. K., JESSEN F., DUNHAM P. B.The Na-K-2Cl cotransporter is in a permanently activated state in cytoplasts from Ehrlich ascites tumor cells.J. Membr. Biol.1381994229239
Crossref | PubMed | ISI | Google Scholar
542 HOFFMANN E. K., JORGENSEN N. K., THOROED S. M., PEDERSEN S., LAMBERT I. H.Role of phospholipase A₂ , leukotrienes, and calcium in volume regulation in Ehrlich ascites tumor cells.J. Physiol. (Lond.)4891995115125
Google Scholar
543 HOFFMANN E. K., LAMBERT I. H., SIMONSEN L. O.Separate, Ca²⁺-activated K⁺ and Cl⁻ transport pathways in Ehrlich ascites tumor cells.J. Membr. Biol.911986227244
Crossref | PubMed | ISI | Google Scholar
544 HOFFMANN E. K., LAMBERT I. H., SIMONSEN L. O.Mechanisms in volume regulation in Ehrlich ascites tumor cells.Renal Physiol. Biochem.111988221247
PubMed | Google Scholar
545 HOFFMANN E. K., SIMONSEN L. O.Membrane mechanisms in volume and pH regulation in vertebrate cells.Physiol. Rev.691989315382
Link | ISI | Google Scholar
546 HOFFMANN E. K., SIMONSEN L. O., LAMBERT I. H.Volume-induced increase of K⁺ and Cl⁻ permeabilities in Ehrlich ascites tumor cells. Role of internal Ca²⁺.J. Membr. Biol.781984211222
Crossref | PubMed | ISI | Google Scholar
547 HOFFMANN, E. K., L. O. SIMONSEN, and I. H. LAMBERT. Cell volume regulation: intracellular transmission. In: Advances in Comparative and Environmental Physiology. Interaction, Cell Volume, Cell Function, edited by F. Lang and D. Häussinger. Berlin: Springer, 1993, vol. 14, p. 187–248.
Google Scholar
548 HOFFMANN E. K., SJOHOLM C., SIMONSEN L. O.Na⁺,Cl⁻ cotransport in Ehrlich ascites tumor cells activated during volume regulation (regulatory volume increase).J. Membr. Biol.761983269280
Crossref | PubMed | ISI | Google Scholar
549 HOFFMANN, E. K., and H. H. USSING. Membrane mechanisms in volume regulation in vertebrate cells and epithelia. In: Membrane Transport in Biology, edited by G. H. Giebisch, J. A. Schafer, H. H. Ussing, and P. Kristensen. Heidelberg, Germany: Springer-Verlag, 1992, vol. 5, p. 317–399.
Google Scholar
550 HOLLMANN M., BOULTER J., MARON C., HEINEMANN S.Molecular biology of glutamate receptors. Potentiation of N-methyl-d-aspartate receptor splice variants by zinc.Renal Physiol. Biochem.171994182183
PubMed | Google Scholar
551 HORN T., BAUCE L., LANDGRAF R., PITTMAN Q. J.Microdialysis with high NaCl causes central release of amino acids and dopamine.J. Neurochem.64199516321644
Crossref | PubMed | ISI | Google Scholar
552 HORTON J. W.Cardiac contractile effects of ethanolism and hemorrhagic shock.Am. J. Physiol.262(Heart Circ. Physiol. 31)1992H1096H1103
Google Scholar
553 HOWARD, R. L., D. G. BICHET, and R. W. SCHRIER. Hypernatremic and polyuric states. In: The Kidney: Physiology and Pathophysiology (2nd ed.), edited by D. W. Seldin and G. Giebisch. New York: Raven, 1992, p. 1753–1778.
Google Scholar
554 HUDSON D. A.Constitutive protein secretion by guinea-pig seminal vesicle epithelial cells.Comp. Biochem. Physiol.1021992701706
Google Scholar
555 HUE L.Control of liver carbohydrate and fatty acid metabolism by cell volume.Biochem. Soc. Trans.221994505508
Crossref | PubMed | ISI | Google Scholar
556 HUNTLEY J. S., HALL A. C., SATHYAMOORTHY V., HALL R. H.Cation flux studies of the lesion induced in human erythrocyte membranes by the thermostable direct hemolysin of Vibrio parahaemolyticus.Infect. Immun.61199343264332
PubMed | ISI | Google Scholar
557 HUNZIKER E. B., WAGNER J., ZAPF J.Differential effects of insulin-like growth factor I and growth hormone on developmental stages of rat growth plate chondrocytes in vivo.J. Clin. Invest.93199410781086
Crossref | PubMed | ISI | Google Scholar
558 HUOT S. J., ARONSON P. S.Na⁺/H⁺ exchanger and its role in essential hypertension and diabetes mellitus.Diabetes Care141991521535
Crossref | PubMed | ISI | Google Scholar
559 HUTTON J. C., SCHOFIELD P. J., WILLIAMS J. F., HOLLOWS F. C.The localisation of sorbitol pathway activity in the rat renal cortex and its relationship to the pathogenesis of the renal complications of diabetes mellitus.Aust. J. Exp. Biol. Med. Sci.5319754957
Crossref | PubMed | Google Scholar
560 HUXTABLE R. J.Physiological actions of taurine.Physiol. Rev.721992101163
Link | ISI | Google Scholar
561 IIMURA O., KUSANO E., ISHIDA F., OONO S., ANDO Y., ASANO Y.Hyperosmolality rapidly reduces atrial-natriuretic-peptide-dependent cyclic guanosine monophosphate production in cultured rat inner medullary collecting duct cells.Pflügers Arch.43019958187
Crossref | PubMed | ISI | Google Scholar
562 INGBER D. E., PRUSTY D., FRANGIONI J. V., CRAGOE E. J.Jr., C. LECHENE, and M. A. SCHWARTZ. Control of intracellular pH and growth by fibronectin in capillary endothelial cells.J. Cell Biol.110199018031811
Crossref | PubMed | ISI | Google Scholar
563 INUKAI T., WANG X., GREER S. E., GREER M. A.Cell swelling induced by medium hyposmolarity or isosmolar urea stimulates gonadotropin-releasing hormone secretion from perifused rat median eminence.Brain Res.5991992161164
Crossref | PubMed | ISI | Google Scholar
564 IRVING T. C., MILLMAN B. M.Z-line/I-band and A-band lattices of intact frog sartorius muscle at altered interfilament spacing.J. Muscle Res. Cell. Motil.131992100105
Crossref | PubMed | ISI | Google Scholar
565 ISHIBASHI K., SASAKI S., FUSHIMI K., UCHIDA S., KUWAHARA M., SAITO H., FURUKAWA T., NAKAJIMA K., YAMAGUCHI Y., GOJOBORI T., MARUMO F.Molecular cloning and expression of a member of the aquaporin family with permeability to glycerol and urea in addition to water expressed at the basolateral membrane of kidney collecting duct cells.Proc. Natl. Acad. Sci. USA91199462696273
Crossref | PubMed | ISI | Google Scholar
566 ITO T., SUZUKI A., STOSSEL T. P.Regulation of water flow by actin-binding protein-induced actin gelation.Biophys. J.61199213011305
Crossref | PubMed | ISI | Google Scholar
567 ITO T., ZANER K. S., STOSSEL T. P.Nonideality of volume flows and phase transitions of F-actin solutions in response to osmotic stress.Biophys. J.511987745753
Crossref | PubMed | ISI | Google Scholar
568 ITOH T., YAMAUCHI A., IMAI E., UEDA N., KAMADA T.Phosphatase toward MAP kinase is regulated by osmolarity in Madin-Darby canine kidney (MDCK) cells.FEBS Lett.3731995123126
Crossref | PubMed | ISI | Google Scholar
569 ITOH T., YAMAUCHI A., MIYAI A., YOKOYAMA K., KAMADA T., UEDA N., FUJIWARA Y.Mitogen-activated protein kinase and its activator are regulated by hypertonic stress in Madin-Darby canine kidney cells.J. Clin. Invest.93199423872392
Crossref | PubMed | ISI | Google Scholar
570 ITZHAK Y., BENDER A. S., NORENBERG M. D.Effect of hypoosmotic stress on peripheral-type benzodiazepine receptors in cultured astrocytes.Brain Res.6441994221225
Crossref | PubMed | ISI | Google Scholar
571 ITZHAK Y., NORENBERG M. D.Ammonia-induced upregulation of peripheral-type benzodiazepine receptors in cultured astrocytes labeled with [³H]PK 11195.Neurosci. Lett.17719943538
Crossref | PubMed | ISI | Google Scholar
572 ITZHAK Y., NORENBERG M. D.Regulation of peripheral-type benzodiazepine receptors in cultured astrocytes by monoamine and amino acid neurotransmitters.Brain Res.6601994346348
Crossref | PubMed | ISI | Google Scholar
573 IYER S. S., PEARSON D. W., NAUSEEF W. M., CLARK R. A.Evidence for a readily dissociable complex of p47phox and p67phox in cytosol of unstimulated human neutrophils.J. Biol. Chem.26919942240522411
PubMed | ISI | Google Scholar
574 JACK R. S.An unusually stable DNA binding protein can locate its specific binding site in the presence of high concentrations of urea.Biochem. Biophys. Res. Commun.1691990840845
Crossref | PubMed | ISI | Google Scholar
575 JACKSON P. S., MORRISON R., STRANGE K.The volume-sensitive organic osmolyte-anion channel VSOAC is regulated by nonhydrolytic ATP binding.Am. J. Physiol.267(Cell Physiol. 36)1994C1203C1209
Link | Google Scholar
576 JACKSON P. S., STRANGE K.Volume-sensitive anion channels mediate swelling-activated inositol and taurine efflux.Am. J. Physiol.265(Cell Physiol. 34)1993C1489C1500
Link | Google Scholar
577 JACOBSON B. S.Interaction of the plasma membrane with the cytoskeleton: an overview.Tissue Cell151983829852
Crossref | PubMed | ISI | Google Scholar
578 JAKUBOVICZ D. E., GRINSTEIN S., KLIP A.Cell swelling following recovery from acidification in C6 glioma cells: an in vitro model of postischemic brain edema.Brain Res.4351987138146
Crossref | PubMed | ISI | Google Scholar
579 JARABAK J., SEEDS A. E.Jr., and P. TALALAY. Reversible cold inactivation of a 17β-hydroxysteroid dehydrogenase of human placenta: protective effect of glycerol.Biochemistry5196612691278
Crossref | ISI | Google Scholar
580 JENNINGS M. L., AL-ROHIL N.Kinetics of activation and inactivation of swelling-stimulated K⁺/Cl⁻ transport. The volume-sensitive parameter is the rate constant for inactivation.J. Gen. Physiol.95199010211040
Crossref | PubMed | ISI | Google Scholar
581 JENNINGS M. L., SCHULZ R. K.Okadaic acid inhibition of KCl cotransport. Evidence that protein dephosphorylation is necessary for activation of transport by either cell swelling or N-ethylmaleimide.J. Gen. Physiol.971991799817
Crossref | PubMed | ISI | Google Scholar
582 JENSEN B. L., SKØTT O.Osmotically sensitive renin release from permeabilized juxtaglomerular cells.Am. J. Physiol.265(Renal Fluid Electrolyte Physiol. 34)1993F87F95
Google Scholar
583 JENSEN B. S., JESSEN F., HOFFMANN E. K.Na⁺,K⁺,Cl⁻ cotransport and its regulation in Ehrlich ascites tumor cells. Ca²⁺/calmodulin and protein kinase C dependent pathways.J. Membr. Biol.1311993161178
Crossref | PubMed | ISI | Google Scholar
584 JENTSCH T. J.Chloride channels: a molecular perspective.Curr. Opin. Neurobiol.61996303310
Crossref | PubMed | ISI | Google Scholar
585 JENTSCH T. J.Molecular physiology of anion channels.Curr. Opin. Cell. Biol.61994600606
Crossref | PubMed | ISI | Google Scholar
586 JESSEN F., HOFFMANN E. K.Activation of the Na⁺/K⁺/Cl⁻ cotransport system by reorganization of the actin filaments in Ehrlich ascites tumor cells.Biochim. Biophys. Acta11101992199201
Crossref | PubMed | ISI | Google Scholar
587 JIANG L. W., CHERNOVA M. N., ALPER S. L.Secondary regulatory volume increase conferred in Xenopus oocytes by expression of AE2 anion exchanger.Am. J. Physiol.272(Cell Physiol. 41)1997C191C202
Link | Google Scholar
588 JIANG L.-W., MAHER V. M., McCORMICK J. J., SCHINDLER M.Alkalinization of the lysosomes is correlated with ras transformation of murine and human fibroblasts.J. Biol. Chem.265199047754777
PubMed | ISI | Google Scholar
589 JIRSCH J., DEELEY R. G., COLE S. P. C., STEWART A. J., FEDIDA D.Inwardly rectifying K⁺ channels and volume-regulated anion channels in multidrug-resistant small cell lung cancer cells.Cancer Res.53199341564160
PubMed | ISI | Google Scholar
590 JIRSCH J. D., LOE D. W., COLE S. P. C., DEELEY R. G., FEDIDA D.ATP is not required for anion current activated by cell swelling in multidrug-resistant lung cancer cells.Am. J. Physiol.267(Cell Physiol. 36)1994C688C699
Link | Google Scholar
591 JOINER C. H.Cation transport and volume regulation in sickle red blood cells.Am. J. Physiol.264(Cell Physiol. 33)1993C251C270
Link | Google Scholar
592 JÖRGENSEN N. K., LAMBERT I. H., HOFFMANN E. K.Role of LTD₄ in the regulatory volume decrease response in Ehrlich ascites tumor cells.J. Membr. Biol.1511996159173
Crossref | PubMed | ISI | Google Scholar
593 JURKOWITZ-ALEXANDER M. S., ALTSCHULD R. A., HOHL C. M., JOHNSON J. D., McDONALD J. S., SIMMONS T. D., HORROCKS L. A.Cell swelling, blebbing, and death are dependent on ATP depletion and independent of calcium during chemical hypoxia in a glial cell line (ROC-1).J. Neurochem.591992344352
Crossref | PubMed | ISI | Google Scholar
594 JUURLINK B. H., CHEN Y., HERTZ L.Use of cell cultures to differentiate among effects of various ischemia factors on astrocytic cell volume.Can. J. Physiol. Pharmacol.70, Suppl.1992S344S349
Crossref | PubMed | ISI | Google Scholar
595 KAJI D. M., DIAZ J., PARKER J. C.Urea inhibits Na-K-2Cl cotransport in medullary thick ascending limb cells.Am. J. Physiol.272(Cell Physiol. 41)1997C615C621
Link | Google Scholar
596 KAJI D. M., GASSON C.Urea activation of K-Cl transport in human erythrocytes.Am. J. Physiol.268(Cell Physiol. 37)1995C1018C1025
Link | Google Scholar
597 KAJI D. M., TSUKITANI Y.Role of protein phosphatase in activation of KCl cotransport in human erythrocytes.Am. J. Physiol.260(Cell Physiol. 29)1991C178C182
Google Scholar
598 KAKINUMA Y., SAKAMAKI Y., ITO K., CRAGOE E. J.Jr., and K. IGARASHI. Relationship among activation of the Na⁺/H⁺ antiporter, ornithine decarboxylase induction, and DNA synthesis.Arch. Biochem. Biophys.2591987171178
Crossref | PubMed | ISI | Google Scholar
599 KANEKO M., CARPER D., NISHIMURA C., MILLEN J., BOCK M., HOHMAN T. C.Induction of aldose reductase expression in rat kidney mesangial cells and Chinese hamster ovary cells under hypertonic conditions.Exp. Cell Res.1881990135140
Crossref | PubMed | ISI | Google Scholar
600 KANLI H., TERREROS D. A.Acute ethanol effects on cell volume regulation.Ann. Clin. Lab. Sci.201990205213
PubMed | ISI | Google Scholar
601 KAPUS A., GRINSTEIN S., WASAN S., KANDASAMY R., ORLOWSKI J.Functional characterization of three isoforms of the Na⁺/H⁺ exchanger stably expressed in Chinese hamster ovary cells.J. Biol. Chem.26919942354423552
PubMed | ISI | Google Scholar
602 KATAOKA S., FUJITA Y.Basal experiments of active oxygen generation in urinary polymorphonuclear leukocytes.Nippon. Hinyokika. Gakkai. Zasshi.8219911623
PubMed | Google Scholar
603 KATAYAMA S., ABE M., TANAKA K., OMOTO A., NEGISHI K., ITABASHI A., ISHII J.High glucose concentration suppresses mesangial laminin B₂ gene expression.J. Diabetic Complications51991118120
Crossref | PubMed | Google Scholar
604 KATZ U.Strategies of adaptation to osmotic stress in anuran amphibia under salt and burrowing conditions.Comp. Biochem. Physiol. A Physiol.931989499503
Crossref | ISI | Google Scholar
605 KAWAHARA K., OGAWA A., SUZUKI M.Hyposmotic activation of Ca-activated K channels in cultured rabbit kidney proximal tubule cells.Am. J. Physiol.260(Renal Fluid Electrolyte Physiol. 29)1991F27F33
Google Scholar
606 KEATING J. P., SHEARS G. J., DODGE P. R.Oral water intoxication in infants: an American epidemic.Am. J. Dis. Child.1451991985990
Crossref | PubMed | Google Scholar
607 KELLEY L. L., KOURY M. J., BONDURANT M. C., KOURY S. T., SAWYER S. T., WICKREMA A.Survival or death of individual proerythroblasts results from differing erythropoietin sensitivities: a mechanism for controlled rates of erythrocyte production.Blood82199323402352
PubMed | ISI | Google Scholar
608 KELLY S. M., MACKLEM P. T.Direct measurement of intracellular pressure.Am. J. Physiol.260(Cell Physiol. 29)1991C652C657
Link | Google Scholar
609 KEMPSKI O., CHAUSSY L., GROSS U., ZIMMER M., BAETHMANN A.Volume regulation and metabolism of suspended C6 glioma cells: an in vitro model to study cytotoxic brain edema.Brain Res.2791983217228
Crossref | PubMed | ISI | Google Scholar
610 KEMPSKI O., SPATZ M., VALET G., BAETHMANN A.Cell volume regulation of cerebrovascular endothelium in vitro.J. Cell. Physiol.12319855154
Crossref | PubMed | ISI | Google Scholar
611 KEMPSKI O., STAUB F., JANSEN M., SCHÖDEL F., BAETHMANN A.Glial swelling during extracellular acidosis in vitro.Stroke191988385392
Crossref | PubMed | ISI | Google Scholar
612 KEMPSKI O., VON ROSEN S., WEIGT H., STAUB F., PETERS J., BAETHMANN A.Glial ion transport and volume control.Ann. NY Acad. Sci.6331991306317
Crossref | PubMed | ISI | Google Scholar
613 KEMPSKI O., ZIMMER M., NEU A., VON ROSEN F., JANSEN M., BAETHMANN A.Control of glial cell volume in anoxia. In vitro studies on ischemic cell swelling.Stroke181987623628
Crossref | PubMed | ISI | Google Scholar
614 KERN T. S., ENGERMAN R. L.Immunohistochemical distribution of aldose reductase.Histochem. J.141982507515
Crossref | PubMed | Google Scholar
615 KERSTING U., NAPATHORN S., SPRING K. R.Necturus gallbladder epithelial cell volume regulation and inhibitors of arachidonic acid metabolism.J. Membr. Biol.13519931118
Crossref | PubMed | ISI | Google Scholar
616 KERSTING U., WOJNOWSKI L., STEIGNER W., OBERLEITHNER H.Hypotonic stress-induced release of KHCO₃ in fused renal epitheloid (MDCK) cells.Kidney Int.391991891900
Crossref | PubMed | ISI | Google Scholar
617 KERR J. F., WYLLIE A. H., CURRIE A. R.Apoptosis: a basic biological phenomenon with wide ranging implications in tissue kinetics.Br. J. Cancer261972239257
Crossref | PubMed | ISI | Google Scholar
618 KHALBUSS W. E., WONDERGEM R.An electrophysiological technique to measure change in hepatocyte water volume.Biochim. Biophys. Acta102919905160
Crossref | PubMed | ISI | Google Scholar
619 KHALBUSS W. E., WONDERGEM R.Involvement of cell calcium and transmembrane potential in control of hepatocyte volume.Hepatology131991962969
Crossref | PubMed | ISI | Google Scholar
620 KIKKAWA R., HANEDA M., TOGAWA M., KOYA D., KAJIWARA N., SHIGETA Y.Differential modulation of mitogenic and metabolic actions of insulin like growth factor I in rat glomerular mesangial cells in high glucose culture.Diabetologia361993276281
Crossref | PubMed | ISI | Google Scholar
621 KILBOURNE E. J., McMAHON A., SABBAN E. L.Membrane depolarization by isotonic or hypertonic KCl: differential effects on mRNA levels of tyrosine hydroxylase and dopamine beta-hydroxylase mRNA in PC12 cells.J. Neurosci. Methods401991193202
Crossref | PubMed | ISI | Google Scholar
622 KIM D., SLADEK C. D., AGUADO-VELASCO C., MATHIASEN J. R.Arachidonic acid activation of a new family of K⁺ channels in cultured rat neuronal cells.J. Physiol. (Lond.)4841995643660
Crossref | Google Scholar
623 KIM Y.-J., SAH R. L. Y., GRODZINSKY A. J., PLAAS A. H. K., SANDY J. D.Mechanical regulation of cartilage biosynthetic behavior: physical stimuli.Arch. Biochem. Biophys.3111994112
Crossref | PubMed | ISI | Google Scholar
624 KIMELBERG H. K.Current concepts of brain edema. Review of Laboratory Investigations.J. Neurosurg.83199510511059
Crossref | PubMed | ISI | Google Scholar
625 KIMELBERG, H. K. Swelling and volume control in brain astroglial cells. In: Advances in Comparative and Environmental Physiology: Volume and Osmolality Control in Animal Cells, edited by R. Gilles, E. K. Hoffmann, and L. Bolis. Berlin: Springer-Verlag, 1991, vol. 9, p. 81–117.
Google Scholar
626 KIMELBERG H. K., GODERIE S. K., HIGMAN S., PANG S., WANIEWSKI R. A.Swelling-induced release of glutamate, aspartate, and taurine from astrocyte cultures.J. Neurosci.10199015831591
Crossref | PubMed | ISI | Google Scholar
627 KIMELBERG H. K., O'CONNOR E. R.Swelling of astrocytes causes membrane potential depolarization.Glia11988219224
Crossref | PubMed | ISI | Google Scholar
628 KIMELBERG H. K., RUTLEDGE E., GODERIE S., CHARNIGA C.Astrocytic swelling due to hypotonic or high K⁺ medium causes inhibition of glutamate and aspartate uptake and increases their release.J. Cereb. Blood Flow Metab.151995409416
Crossref | PubMed | ISI | Google Scholar
629 KINNE R. K. H.The role of organic osmolytes in osmoregulation: from bacteria to mammals.J. Exp. Zool.2651993346355
Crossref | PubMed | Google Scholar
630 KINNE R. K. H., CZEKAY R. P., GRUNEWALD J. M., MOOREN F. C., KINNE-SAFFRAN E.Hypotonicity-evoked release of organic osmolytes from distal renal cells: systems, signals, and sidedness.Renal Physiol. Biochem.1619936678
PubMed | Google Scholar
631 KIRK K. L., DIBONA D. R., SCHAFER J. A.Regulatory volume decrease in perfused proximal nephron: evidence for a dumping of cell K⁺.Am. J. Physiol.252(Renal Fluid Electrolyte Physiol. 21)1987F933F942
Google Scholar
632 KIRK K., ELLORY J. C., YOUNG J. D.Transport of organic substrates via a volume-activated channel.J. Biol. Chem.26719922347523478
PubMed | ISI | Google Scholar
633 KIRK K., HORNER H. A.Novel anion dependence of induced cation transport in malaria-infected erythrocytes.J. Biol. Chem.27019952427024275
Crossref | PubMed | ISI | Google Scholar
634 KIRK K. L., SCHAFER J. A., DIBONA D. R.Cell volume regulation in rabbit proximal straight tubule perfused in vitro.Am. J. Physiol.252(Renal Fluid Electrolyte Physiol. 21)1987F922F932
Google Scholar
635 KLEIN J. D., O'NEILL W. C.Volume-sensitive myosin phosphorylation in vascular endothelial cells: correlation with Na-K-2Cl cotransport.Am. J. Physiol.269(Cell Physiol. 38)1995C15241531
Link | Google Scholar
636 KLEIN J. D., PERRY P. B., O'NEILL W. C.Regulation by cell volume of Na⁺-K⁺-2Cl⁻ cotransport in vascular endothelial cells: role of protein phosphorylation.J. Membr. Biol.1321993243252
Crossref | PubMed | ISI | Google Scholar
637 KLEINZELLER A., BOOZ G. W., MILLS J. W., ZIYADEH F. N.pCMBS-induced swelling of the dogfish (Squalus acanthias) rectal gland cells: role of the Na⁺,K⁺-ATPase and the cytoskeleton.Biochim. Biophys. Acta102519902131
Crossref | PubMed | ISI | Google Scholar
638 KLEINZELLER A., MILLS J. W.K⁺-induced swelling of the dogfish shark (Squalus acanthias) rectal gland cells is associated with changes of the cytoskeleton.Biochim. Biophys. Acta101419894052
Crossref | PubMed | ISI | Google Scholar
639 KOCH-JENSEN P., FISHER R. S., SPRING K. R.Feedback inhibition of NaCl entry in Necturus gallbladder epithelial cells.J. Membr. Biol.82198495104
Crossref | PubMed | ISI | Google Scholar
640 KOHAN D. E., PADILLA E.Osmolar regulation of endothelin-1 production by rat inner medullary collecting duct.J. Clin. Invest.91199312351240
Crossref | PubMed | ISI | Google Scholar
641 KOLB H. A., UBL J.Activation of anion channels by zymosan particles in membranes of peritoneal macrophages.Biochim. Biophys. Acta8991987239246
Crossref | PubMed | ISI | Google Scholar
642 KOLENA J., MATEJCIKOVA K., SRENKELOVA G.Osmolytes improve the reconstitution of luteinizing hormone/human chorionic gonadotropin receptors into proteoliposomes.Mol. Cell. Endocrinol.831992201209
Crossref | PubMed | ISI | Google Scholar
643 KOPELMAN H., GAUTHIER C., BORNSTEIN M.Antisense oligodeoxynucleotide to the cystic fibrosis transmembrane conductance regulator inhibits cyclic AMP-activated but not calcium-activated cell volume reduction in a human pancreatic duct cell line.J. Clin. Invest.91199312531257
Crossref | PubMed | ISI | Google Scholar
644 KRÄMER-GUTH A., SCHWEDLER S., BUSCH G. L., KÜPPER B., LANG F., WANNER C.Effect of osmolarity on LDL binding and internalization in hepatocytes.Am. J. Physiol.273(Cell Physiol. 42)1997C1409C1415
Link | Google Scholar
645 KRAMHØFT B., HOFFMANN E. K., SIMONSEN L. O.pH_i regulation in Ehrlich mouse ascites tumor cells: role of sodium-dependent and sodium-independent chloride-bicarbonate exchange.J. Membr. Biol.1381994121132
Crossref | PubMed | ISI | Google Scholar
646 KRANE E. J., ROCKOFF M. A., WALLMAN J. K., WOLFSDORF J. I.Subclinical brain swelling in children during treatment of diabetic ketoacidosis.N. Engl. J. Med.312198511471151
Crossref | PubMed | ISI | Google Scholar
647 KRAPIVINSKY, G. B., M. J. ACKERMAN, E. A. GORDON, L. D. KRAPIVINSKY, and D. E. CLAPHAM. Molecular characterization of a swelling induced chloride conductance regulatory protein, plCln Cell 76: 439–448, 1994.
Google Scholar
648 KREGENOW F. M., ROBBIE D. E., ORLOFF J.Effect of norepinephrine and hypertonicity on K influx and cyclic AMP in duck erythrocytes.Am. J. Physiol.2311976306311
Abstract | ISI | Google Scholar
649 KREIS R., FARROW N., ROSS B. D.Localized ¹H NMR sprectroscopy in patients with chronic hepatic encephalopathy. Analysis of changes in cerebral glutamine, choline and inositols.NMR Biomed.41991109116
Crossref | PubMed | ISI | Google Scholar
650 KREIS R., ROSS B. D., FARROW N. A., ACKERMAN Z.Metabolic disorders of the brain in chronic hepatic encephalopathy detected with H-1 MR spectroscopy.Radiology18219921927
Crossref | PubMed | ISI | Google Scholar
651 KRIPPEIT-DREWS P., HABERLAND C., FINGERLE J., DREWS G., LANG F.Effects of H₂O₂ on membrane potential and [Ca²⁺]_i of cultured rat arterial smooth muscle cells.Biochem. Biophys. Res. Commun.2091995139145
Crossref | PubMed | ISI | Google Scholar
652 KRIPPEIT-DREWS P., LANG F., HÄUSSINGER D., DREWS G.H₂O₂ induced hyperpolarization of pancreatic B-cells.Pflügers Arch.4261994552554
Crossref | PubMed | ISI | Google Scholar
653 KRISTENSEN L. O.Associations between transports of alanine and cations across cell membrane in rat hepatocytes.Am. J. Physiol.251(Gastrointest. Liver Physiol. 14)1986G575G584
Google Scholar
654 KRISTENSEN L. O., FOLKE M.Volume-regulatory K⁺ efflux during concentrative uptake of alanine in isolated rat hepatocytes.Biochem. J.2211984265268
Crossref | PubMed | ISI | Google Scholar
655 KRÖNKE M., SCHÜTZE S., WIEGMANN K., MACHLEIDT T.Sphingomyelinases and TNF-induced apoptosis.Cell. Physiol. Biochem.61996337344
Crossref | ISI | Google Scholar
656 KRUPPA J., CLEMENS M. J.Differential kinetics of changes in the state of phosphorylation of ribosomal protein S6 and in the rate of protein synthesis in MPC 11 cells during tonicity shifts.EMBO J.3198495100
Crossref | PubMed | ISI | Google Scholar
657 KUBO M., OKADA Y.Volume-regulatory Cl⁻ channel current in cultured human epithelial cells.J. Physiol. (Lond.)4561992351371
Crossref | Google Scholar
658 KUCHKINA N. V., ORLOV S. N., POKUDIN N. I., CHUCHALIN A. G.Effect of osmolarity of the medium on the chemiluminescence of human neutrophils.Biul. Eksp. Biol. Med.1151993360362
PubMed | Google Scholar
659 KUCHKINA N. V., ORLOV S. N., POKUDIN N. I., CHUCHALIN A. G.Volume-dependent regulation of the respiratory burst of activated human neutrophils.Experientia491993995997
Crossref | PubMed | Google Scholar
660 KUHLENSCHMIDT M. S., HOFFMANN W. E., RIPPY M. K.Glucocorticoid hepatopathy: effect on receptor-mediated endocytosis of asialoglycoproteins.Biochem. Med. Metab. Biol.461991152168
Crossref | PubMed | Google Scholar
661 KUHN J. L., DELACY J. H., LEENELLETT E. E.Relationship between bone growth rate and hypertrophic chondrocyte volume in New Zealand White rabbits of varying ages.J. Orthoped. Res.141996706711
Crossref | PubMed | ISI | Google Scholar
662 KUMAZAWA Y., ARAI K.Suppressive effect of sorbitol on denaturation of carp myosin B induced by neutral salts.Nippon Suisan Gakkaishi.561990679686
Crossref | ISI | Google Scholar
663 KUNZELMANN K., SLOTKI I. N., KLEIN P., KOSLOWSKY T., AUSIELLO D. A., GREGER R., CABANTCHIK Z. I.Effects of P-glycoprotein expression on cyclic AMP and volume-activated ion fluxes and conductances in HT-29 colon adenocarcinoma cells.J. Cell. Physiol.1611994393406
Crossref | PubMed | ISI | Google Scholar
664 KURIYAMA S., KAGUCHI Y., NAKAMURA K., HASHIMOTO T., SAKAI O.Effect of serum on cell membrane Na-K transport of vascular smooth muscle in culture — a comparative study between normotensive and hypertensive rats.Pharmacol. Res.251992155165
PubMed | ISI | Google Scholar
665 KURTZ, A. Do calcium-activated chloride channels control renin secretion? News Physiol. Sci. 5: 43–46, 1990.
Google Scholar
666 KWON, H. M. Molecular regulation of mammalian osmolyte transporters. In: Cellular and Molecular Physiology of Cell Volume Regulation, edited by K. Strange. Boca Raton, FL: CRC, 1994, p. 383–394.
Google Scholar
667 KWON H. M.Osmoregulation of Na-coupled organic osmolyte transporters.Renal Physiol. Biochem.171994205207
PubMed | Google Scholar
668 KWON H. M., HANDLER J. S.Cell volume regulated transporters of compatible osmolytes.Curr. Opin. Cell Biol.71995465471
Crossref | PubMed | ISI | Google Scholar
669 KWON H. M., ITOH T., RIM J. S., HANDLER J. S.The MAP kinase cascade is not essential for transcriptional stimulation of osmolyte transporter genes.Biochem. Biophys. Res. Commun.2131995975979
Crossref | PubMed | ISI | Google Scholar
670 KWON H. M., YAMAUCHI A., UCHIDA S., PRESTON A. S., GARCIA-PEREZ A., BURG M. B., HANDLER J. S.Cloning of the cDNA for a Na⁺/myo-inositol cotransporter, a hypertonicity stress protein.J. Biol. Chem.267199262976301
PubMed | ISI | Google Scholar
671 LAMBERT I. H.Na⁺-dependent taurine uptake in Ehrlich ascites tumor cells.Mol. Physiol.61984233246
Google Scholar
672 LAMBERT I. H.Taurine transport in Ehrlich ascites tumor cells. Specificity and chloride dependence.Mol. Physiol.71985323332
Google Scholar
673 LAMBERT I. H.Effect of arachidonic acid, fatty acids, prostaglandins, and leukotrienes on volume regulation in Ehrlich ascites tumor cells.J. Membr. Biol.981987207221
Crossref | PubMed | ISI | Google Scholar
674 LAMBERT I. H.Leukotriene-D₄ induced cell shrinkage in Ehrlich ascites tumor cells.J. Membr. Biol.1081989165176
Crossref | PubMed | ISI | Google Scholar
675 LAMBERT, I. H. Eicosanoids and cell volume regulation. In: Cellular and Molecular Physiology of Cell Volume Regulation, edited by K. Strange. Boca Raton, FL: CRC, 1994, p. 279–298.
Google Scholar
676 LAMBERT I. H., HOFFMANN E. K.Amino acid metabolism and protein turnover under different osmotic conditions in Ehrlich ascites tumor cells.Mol. Physiol.21982273286
Google Scholar
677 LAMBERT I. H., HOFFMANN E. K.Cell swelling activates separate taurine and chloride channels in Ehrlich mouse ascites tumor cells.J. Membr. Biol.1421994289298
Crossref | PubMed | ISI | Google Scholar
678 LAMBERT I. H., HOFFMANN E. K.Regulation of taurine transport in Ehrlich ascites tumor cells.J. Membr. Biol.13119936779
Crossref | PubMed | ISI | Google Scholar
679 LAMBERT I. H., HOFFMANN E. K., CHRISTENSEN P.Role of prostaglandins and leukotrienes in volume regulation by Ehrlich ascites tumor cells.J. Membr. Biol.981987247256
Crossref | PubMed | ISI | Google Scholar
680 LAMBERT I. H., HOFFMANN E. K., JØRGENSEN F.Membrane potential, anion and cation conductances in Ehrlich ascites tumor cells.J. Membr. Biol.1111989113131
Crossref | PubMed | ISI | Google Scholar
681 LANG F., BUSCH G. L., GULBINS E.Physiology of cell survival and cell death: implications for organ conservation.Nephrol. Dial. Transplant.10199515511555
PubMed | ISI | Google Scholar
682 LANG F., BUSCH G. L., VÖLKL H.The diversity of volume regulatory mechanisms.Cell. Physiol. Biochem.81998145
Crossref | PubMed | ISI | Google Scholar
683 LANG F., BUSCH G. L., VÖLKL H., HÄUSSINGER D.Lysosomal pH: a link between cell volume and metabolism.Biochem. Soc. Trans.221994502505
Crossref | PubMed | ISI | Google Scholar
684 LANG F., BUSCH G. L., VÖLKL H., HÄUSSINGER D.Cell volume: a second message in regulation of cellular function.News Physiol. Sci.1019951822
Abstract | Google Scholar
685 LANG F., BUSCH G. L., ZEMPEL G., DITLEVSEN J., HOCH M., EMERICH U., AXEL D., FINGERLE J., MEIERKORD S., APFEL H., KRIPPEIT-DREWS P., HEINLE H.Ca²⁺ entry and vasoconstriction during osmotic swelling of vascular smooth muscle cells.Pflügers Arch.4311995253258
Crossref | PubMed | ISI | Google Scholar
686 LANG F., FRIEDRICH F., KAHN E., WÖLL E., HAMMERER M., WALDEGGER S., MALY K., GRUNICKE H.Bradykinin-induced oscillations of cell membrane potential in cells expressing the Ha-ras oncogene.J. Biol. Chem.266199149384942
PubMed | ISI | Google Scholar
686a LANG, F., J. MADLUNG, and E. GULBINS. Stimulation of taurine release during Fas-(CD95)-induced apoptotic cell death (Abstract). Pflügers Arch. In press.
Google Scholar
687 LANG F., MESSNER G., REHWALD W.Electrophysiology of sodium-coupled transport in proximal renal tubules.Am. J. Physiol.250(Renal Fluid Electrolyte Physiol. 19)1986F953F962
Google Scholar
688 LANG F., MESSNER G., WANG W., OBERLEITHNER H.Interaction of intracellular electrolytes and tubular transport.Klin. Wochenschr.61198310291037
Crossref | PubMed | Google Scholar
689 LANG, F., H. OBERLEITHNER, H. A. KOLB, M. PAULMICHL, H. VÖLKL, and W. WANG. Interaction of intracellular pH and cell membrane potential. In: pH Homeostasis: Mechanisms and Control, edited by D. Häussinger. San Diego, CA: Academic, 1988, p. 27–42.
Google Scholar
690 LANG F., PAULMICHL M.Properties and regulation of ion channels in MDCK cells.Kidney Int.48199512001205
Crossref | PubMed | ISI | Google Scholar
691 LANG, F., M. PAULMICHL, H. VÖLKL, E. GSTREIN, and F. FRIEDRICH. Electrophysiology of cell volume regulation. In: Molecular Physiology: Biochemical Aspects of Kidney Function, edited by Z. Kovacevic and W. G. Guder. Berlin: de Gruyter, 1987, p. 133–139.
Google Scholar
692 LANG F., REHWALD W.Potassium channels in renal epithelial transport regulation.Physiol. Rev.721992132
Link | ISI | Google Scholar
693 LANG F., RITTER M., VÖLKL H., HÄUSSINGER D.The biological significance of cell volume.Renal Physiol. Biochem.1619934865
PubMed | Google Scholar
694 LANG F., RITTER M., WÖLL E., BICHLER I., HÄUSSINGER D., OFFNER F., GRUNICKE H.Ion transport in the regulation of cell proliferation in ras oncogene expressing 3T3 NIH fibroblasts.Cell. Physiol. Biochem21992213224
Crossref | Google Scholar
695 LANG F., RITTER M., WÖLL E., WEISS H., HÄUSSINGER D., HOFLACHER J., MALY K., GRUNICKE H.Altered cell volume regulation in ras oncogene expressing NIH fibroblasts.Pflügers Arch.4201992424427
Crossref | PubMed | ISI | Google Scholar
696 LANG F., STEHLE T., HÄUSSINGER D.Water, K⁺, H⁺, lactate and glucose fluxes during cell volume regulation in perfused rat liver.Pflügers Arch.4131989209216
Crossref | PubMed | ISI | Google Scholar
697 LANG F., WALDEGGER S., WÖLL E., RITTER M., MALY K., GRUNICKE H.Effects of inhibitors and ion substitutions on oscillations of cell membrane potential in cells expressing the ras oncogene.Pflügers Arch.4211992416424
Crossref | PubMed | ISI | Google Scholar
698 LANYI J. K.Salt-dependent properties of proteins from extremely halophilic bacteria.Bacteriol. Rev.381974272290
PubMed | Google Scholar
699 LARCOMBE-McDOUALL J. B., SEO Y., STEWARD M. C.Continuous measurement of cell volume changes in perfused rat salivary glands by proton NMR.Magn. Reson. Med.311994131138
Crossref | PubMed | ISI | Google Scholar
700 LARKIN J. M., BROWN M. S., GOLDSTEIN J. L., ANDERSON R. G.Depletion of intracellular potassium arrests coated pit formation and receptor-mediated endocytosis in fibroblasts.Cell331983273285
Crossref | PubMed | ISI | Google Scholar
701 LARKIN J. M., DONZELL W. C., ANDERSON R. G.Potassium-dependent assembly of coated pits: new coated pits form as planar clathrin lattices.J. Cell Biol.103198626192627
Crossref | PubMed | ISI | Google Scholar
702 LARSEN A. K., JENSEN B. S., HOFFMANN E. K.Activation of protein kinase C during cell volume regulation in Ehrlich mouse ascites tumor cells.Biochim. Biophys. Acta12221994477482
Crossref | PubMed | ISI | Google Scholar
703 LASSING I., LINDBERG U.Specific interaction between phosphatidylinositol 4,5-bisphosphate and profilactin.Nature3141985472474
Crossref | PubMed | ISI | Google Scholar
704 LASSING I., LINDBERG U.Specificity of the interaction between phosphatidylinositol 4,5-bisphosphate and the profilin-actin complex.J. Cell Biochem.371988255267
Crossref | PubMed | ISI | Google Scholar
705 LATZKOVITS L., CSERR H. F., PARK J. T., PATLAK C. S., PETTIGREW K. D., RIMANOCZY A.Effects of arginine vasopressin and atriopeptin on glial cell volume measured as 3-MG space.Am. J. Physiol.264(Cell Physiol. 33)1993C603C608
Link | Google Scholar
706 LAU K. R., HUDSON R. L., SCHULTZ S. G.Cell swelling increases a barium-inhibitable potassium conductance in the basolateral membrane of Necturus small intestine.Proc. Natl. Acad. Sci. USA81198435913594
Crossref | PubMed | ISI | Google Scholar
707 LAUER G., MINUTH W. W.Apico-basal osmotic gradient induces transcytosis in cultured renal collecting duct epithelium.J. Membr. Biol.101198893101
Crossref | PubMed | ISI | Google Scholar
708 LAUF P. K.K:Cl cotransport: emerging molecular aspects of a ouabain-resistant, volume-responsive transport system in red blood cells.Renal Physiol. Biochem.111988248259
PubMed | Google Scholar
709 LAUF P. K.On the relationship between volume- and thiol-stimulated K⁺ Cl⁻ fluxes in red cell membranes.Mol. Physiol.81985215234
Google Scholar
710 LAUF P. K.Passive K⁺-Cl⁻ fluxes in low-K⁺ sheep erythrocytes: modulation by A23187 and bivalent cations.Am. J. Physiol.249(Cell Physiol. 18)1985C271C278
Link | Google Scholar
711 LAUF P. K., ERDMANN A., ADRAGNA N. C.K-Cl cotransport, pH, and role of Mg in volume-clamped low-K sheep erythrocytes: three equilibrium states.Am. J. Physiol.266(Cell Physiol. 35)1994C95C103
Link | Google Scholar
712 LAURITZEN L., HOFFMANN E. K., HANSEN H. S., JENSEN B.Dietary n-3 and n-6 fatty acids are equipotent in stimulating volume regulation in Ehrlich ascites tumor cells.Am. J. Physiol.264(Cell Physiol. 33)1993C109C117
Link | Google Scholar
713 LAVOINNE A., HUSSON A., QUILLARD M., CHEDEVILLE A., FAIRAND A.Glutamine inhibits the lowering effect of glucose on the level of phosphoenolpyruvate carboxykinase mRNA in isolated rat hepatocytes.Eur. J. Biochem.2421996537543
Crossref | PubMed | Google Scholar
714 LAW R. O.Amino acids as volume-regulatory osmolytes in mammalian cells.Comp. Biochem. Physiol. A Physiol.991991263277
Crossref | ISI | Google Scholar
715 LAW R. O.Effects of extracellular bicarbonate ions and pH on volume-regulatory taurine efflux from rat cerebral cortical slices in vitro: evidence for separate neutral and anionic transport mechanisms.Biochim. Biophys. Acta12241994377383
Crossref | PubMed | ISI | Google Scholar
716 LAW R. O.Regulation of mammalian brain cell volume.J. Exp. Zool.26819949096
Crossref | PubMed | Google Scholar
717 LAW R. O.Taurine efflux and the regulation of cell volume in incubated slices of rat cerebral cortex.Biochim. Biophys. Acta122119942128
Crossref | PubMed | ISI | Google Scholar
718 LAW R. O.The volume and ionic composition of cells in incubated slices of rat renal cortex, medulla and papilla.Biochim. Biophys. Acta9311987276285
Crossref | PubMed | ISI | Google Scholar
719 LAW, R. O., and M. B. BURG. The role of organic osmolytes in the regulation of mammalian cell volume. In: Advances in Comparative and Environmental Physiology, edited by R. Gilles. Heidelberg: Springer-Verlag, 1991, p. 189–225.
Google Scholar
720 LAWITTS J. A., BIGGERS J. D.Joint effects of sodium chloride, glutamine, and glucose in mouse preimplantation embryo culture media.Mol. Reprod. Dev.311992189194
Crossref | PubMed | ISI | Google Scholar
721 LEAF A.On the mechanisms of fluid exchange of tissues in vitro.Biochem. J.621956241248
Crossref | PubMed | ISI | Google Scholar
722 LECHENE C.Cellular volume and cytoplasmic gel.Biol. Cell551985177180
Crossref | PubMed | ISI | Google Scholar
723 LEE, J. A., H. A. LEE, and P. J. SADLER. Uraemia: is urea more important than we think? Lancet 338: 1438–1440, 1991.
Google Scholar
724 LEE K. H., LEE S. B., CHO K. C.Levels of organic osmolytes in normal and diuretic rat kidneys.Contrib. Nephrol.951991279283
Crossref | PubMed | Google Scholar
725 LEJBKOWICZ F., SALZBERG S.Biological effects of photoactivated-HPD and cholesteryl hemisuccinate on erythroid differentiation.Biomater. Artif. Cells Immobil. Biotechnol.20199211111120
PubMed | Google Scholar
726 LEONARD R. J., GARCIA M. L., SLAUGHTER R. S., REUBEN J. P.Selective blockers of voltage-gated K⁺ channels depolarize human T lymphocytes: mechanism of the antiproliferative effect of charybdotoxin.Proc. Natl. Acad. Sci. USA8919921009410098
Crossref | PubMed | ISI | Google Scholar
727 LEPIDI H., BENOLIEL A. M., MEGE J. L., BONGRAND P., CAPO C.Double localization of F-actin in chemoattractant-stimulated polymorphonuclear leucocytes.J. Cell Sci.1031992145156
PubMed | ISI | Google Scholar
727a LEPPLE-WIENHUES, A., I. SZABO, T. LAUN, N. K. KABA, E. GULBINS, and F. LANG. The tyrosine kinase p56^lck mediates activation of swelling-induced chloride channels in lymphocytes (Abstract). Pflügers Arch. In press.
Google Scholar
728 LEUNG S., O'DONNELL M. E., MARTINEZ A., PALFREY H. C.Regulation by nerve growth factor and protein phosphorylation of Na/K/2Cl cotransport and cell volume in PC12 cells.J. Biol. Chem.26919941058110589
PubMed | ISI | Google Scholar
729 LEUNIG A., STAUB F., PETERS J., HEIMANN A., CSAPO C., KEMPSKI O., GOETZ A. E.Relation of early Photofrin uptake to photodynamically induced phototoxicity and changes of cell volume in different cell lines.Eur. J. Cancer3019947883
Crossref | ISI | Google Scholar
730 LEUNIG A., STAUB F., PETERS J., LEIDERER R., FEYH J., GOETZ A.Die Schädigung von Tumorzellen durch die photodynamische Therapie.Laryngorhinootologie731994102107
Crossref | PubMed | ISI | Google Scholar
731 LEVI G., PATRIZIO M.Astrocyte heterogeneity: endogenous amino acid levels and release evoked by non-N-methyl-d-aspartate receptor agonists and by potassium-induced swelling in type-1 and type-2 astrocytes.J. Neurochem.58199219431952
Crossref | PubMed | ISI | Google Scholar
732 LEVIEL F., FROISSART M., SOUALMIA H., POGGIOLI J., PAILLARD M., BICHARA M.Control of H⁺-HCO⁻₃ plasma membrane transporters by urea hyperosmolality in rat medullary thick ascending limb.Am. J. Physiol.266(Cell Physiol. 35)1994C1157C1164
Link | Google Scholar
733 LEVIN E. G., SANTELL L., SALJOOQUE F.Hyperosmotic stress stimulates tissue plasminogen activator expression by a PKC-independent pathway.Am. J. Physiol.265(Cell Physiol. 34)1993C387C396
Link | Google Scholar
734 LEVINSON C.Regulatory volume increase in Ehrlich ascites tumor cells.Biochim. Biophys. Acta1021199018
Crossref | PubMed | ISI | Google Scholar
735 LEVINSON C.Inability of Ehrlich ascites tumor cells to volume regulate following a hyperosmotic challenge.J. Membr. Biol.1211991279288
Crossref | PubMed | ISI | Google Scholar
736 LEVITAN I., ALMONTE C., MOLLARD P., GARBER S. S.Modulation of a volume-regulated chloride current by F-actin.J. Membr. Biol.1471995283294
Crossref | PubMed | ISI | Google Scholar
737 LEW V. L., BOOKCHIN R. M.Osmotic effects of protein polymerization: analysis of volume changes in sickle cell anemia red cells following deoxy-hemoglobin S polymerization.J. Membr. Biol.12219915567
Crossref | PubMed | ISI | Google Scholar
738 LEW V. L., BOOKCHIN R. M.Volume, pH, and ion-content regulation in human red cells: analysis of transient behaviour with an integrated model.J. Membr. Biol.9219865774
Crossref | PubMed | ISI | Google Scholar
739 LEWIS R. S., CAHALAN M. D.The plasticity of ion channels: parallels between the nervous and immune systems.Trends Neurosci.111988214218
Crossref | PubMed | ISI | Google Scholar
740 LEWIS S. A., BUTT A. G., BOWLER M. J., LEADER J. P., MACKNIGHT A. D. C.Effects of anions on cellular volume and transepithelial Na⁺ transport across toad urinary bladder.J. Membr. Biol.831985119137
Crossref | PubMed | ISI | Google Scholar
741 LEWIS S. A., DE MOURA J. L.Incorporation of cytoplasmic vesicles into apical membrane of mammalian urinary bladder epithelium.Nature2971982685688
Crossref | PubMed | ISI | Google Scholar
742 LEWIS S. A., EATON D. C., DIAMOND J. M.The mechanism of Na⁺ transport by rabbit urinary bladder.J. Membr. Biol.2819764170
Crossref | PubMed | ISI | Google Scholar
743 LI Q., JUNGMANN V., KIYATKIN A., LOW P. S.Prostaglandin E₂ stimulates a Ca²⁺ dependent K⁺ channel in human erythrocytes and alters cell volume and filterabilty.J. Biol. Chem.27119961865118656
Crossref | PubMed | ISI | Google Scholar
744 LICHTSTEIN D., GATI I., HAVER E., KATZ U.Digitalis-like compounds in the toad Bufo viridis: tissue and plasma levels and significance in osmotic stress.Life Sci.511992119128
Crossref | PubMed | ISI | Google Scholar
745 LIEN Y. H., SHAPIRO J. I., CHAN L.Effects of hypernatremia on organic brain osmoles.J. Clin. Invest.85199014271435
Crossref | PubMed | ISI | Google Scholar
746 LIEN Y. H., SHAPIRO J. I., CHAN L.Study of brain electrolytes and organic osmolytes during correction of chronic hyponatremia. Implications for the pathogenesis of central pontine myelinolysis.J. Clin. Invest.881991303309
Crossref | PubMed | ISI | Google Scholar
747 LIEN Y. H., ZHOU H. Z., JOB C., BARRY J. A., GILLIES R. J.In vivo ³¹P NMR study of early cellular responses to hyperosmotic shock in cultured glioma cells.Biochimie741992931939
Crossref | PubMed | ISI | Google Scholar
748 LIN L. R., REDDY V. N., GIBLIN F. J., KADOR P. F., KINOSHITA J. H.Polyol accumulation in cultured human lens epithelial cells.Exp. Eye Res.52199193100
Crossref | PubMed | ISI | Google Scholar
749 LIN M., MACLEOD K., GUGGINO S.Heat-stable toxin from Escherichia coli activates chloride current via cGMP-dependent protein kinase.Cell Physiol. Biochem.519952332
Crossref | ISI | Google Scholar
750 LIN T. Y., TIMASHEFF S. N.Why do some organisms use a urea-methylamine mixture as osmolyte? Thermodynamic compensation of urea and trimethylamine N-oxide interactions with protein.Biochemistry3319941269512701
Crossref | PubMed | ISI | Google Scholar
751 LING B. N., WEBSTER C. L., EATON D. C.Eicosanoids modulate apical Ca²⁺-dependent K⁺ channels in cultured rabbit principal cells.Am. J. Physiol.263(Renal Fluid Electrolyte Physiol. 32)1992F116F126
Google Scholar
752 LING H., VAMVAKAS S., BUSCH G. L., DÄMMRICH J., SCHRAMM L., LANG F., HEIDLAND A.Suppressing role of transforming growth factor-β1 on cathepsin activity in cultured kidney tubule cells.Am. J. Physiol.269(Renal Fluid Electrolyte Physiol. 38)1995F911F917
Google Scholar
753 LINSHAW M. A.Effect of metabolic inhibitors on renal tubule cell volume.Am. J. Physiol.239(Renal Fluid Electrolyte Physiol. 8)1980F571F577
Google Scholar
754 LINSHAW M. A., FOGEL C. A., DOWNEY G. P., KOO E. W., GOTLIEB A. I.Role of cytoskeleton in volume regulation of rabbit proximal tubules in dilute medium.Am. J. Physiol.262(Renal Fluid Electrolyte Physiol. 31)1992F144F150
Google Scholar
755 LINSHAW M. A., GRANTHAM J. J.Effect of collagenase and ouabain on renal cell volume in hypotonic media.Am. J. Physiol.238(Renal Fluid Electrolyte Physiol. 7)1980F491F498
Google Scholar
756 LIPSCOMBE D., MADISON D. V., POENIE M., REUTER H., TSIEN R. Y., TSIEN R. W.Spatial distribution of calcium channels and cytosolic calcium transients in growth cones and cell bodies of sympathetic neurons.Proc. Natl. Acad. Sci. USA85198823982402
Crossref | PubMed | ISI | Google Scholar
757 LIVNE A., HOFFMANN E. K.Cytoplasmic acidification and activation of Na⁺/H⁺ exchange during regulatory volume decrease in Ehrlich ascites tumor cells.J. Membr. Biol.1141990153157
Crossref | PubMed | ISI | Google Scholar
758 LOHR J. W., ACARA M.Effect of dimethylaminoethanol, an inhibitor of betaine production on the disposition of choline in the rat kidney.J. Pharmacol. Exp. Ther.2521990154158
PubMed | ISI | Google Scholar
759 LOOMIS, S. H., J. F. CARPENTER, and J. H. CROWE. Identification of strombine and taurine as cryoprotectants in the intertidal bivalve Mytilus edulis. Biochim. Biophys. Acta 943: 113–118, 1988.
Google Scholar
760 LORENZ L., PUSCH M., JENTSCH T. J.Heteromultimeric CLC chloride channels with novel properties.Proc. Natl. Acad. Sci. USA9319961336213366
Crossref | PubMed | ISI | Google Scholar
761 LOVKVIST-WALLSTROM E., STJERNBORG-ULVSBACK L., SCHEFFLER I. E., PERSSON L.Regulation of mammalian ornithine decarboxylase. Studies on the induction of the enzyme by hypotonic stress.Eur. J. Biochem.23119954044
Crossref | PubMed | Google Scholar
762 LOW S. Y., RENNIE M. J., TAYLOR P. M.Modulation of glycogen synthesis in rat skeletal muscle by changes in cell volume.J. Physiol. (Lond.)4951996299303
Crossref | Google Scholar
763 LUCHT J. M., BREMER E.Adaptation of Escherichia coli to high osmolarity environments: osmoregulation of the high affinity glycine betaine transport system proU.FEMS Microbiol. Rev.141994320
Crossref | PubMed | ISI | Google Scholar
764 LUCKIE D. B., KROUSE M. E., LAW T. C., SIKIC B. I., WINE F. J.Doxorubicin selection for MDR1/P-glycoprotein reduces swelling-activated K⁺ and Cl⁻ currents in MES-SA cells.Am. J. Physiol.270(Cell Physiol. 39)1996C1029C1036
Link | Google Scholar
765 LUDVIGSON M. A., SORENSON R. L.Immunohistochemical localization of aldose reductase. II. Rat eye and kidney.Diabetes291980450459
Crossref | PubMed | ISI | Google Scholar
766 LUIKEN J. J., AERTS J. M., MEIJER A. J.The role of the intralysosomal pH in the control of autophagic proteolytic flux in rat hepatocytes.Eur. J. Biochem.2351996564573
Crossref | PubMed | Google Scholar
767 LUIKEN, J. J. F. P., E. F. C. BLOMMAART, L. BOON, G. M. VAN WOERKOM, and A. J. MEIJER. Cell swelling and the control of autophagic proteolysis in hepatocytes: involvement of phosphorylation of ribosomal protein S6? Biochem. Soc. Trans. 22: 508–511, 1994.
Google Scholar
768 LUND P. E., BERTS A., HELLMAN B.Stimulation of insulin release by isosmolar addition of permeant molecules.Mol. Cell. Biochem.10919927781
Crossref | PubMed | ISI | Google Scholar
769 LUNDGREN D. W.Effect of hypotonic stress on ornithine decarboxylase mRNA expression in cultured cells.J. Biol. Chem.267199268416847
PubMed | ISI | Google Scholar
770 LÜSCHER T. F.Endothelium in the control of vascular tone and growth: role of local mediators and mechanical forces.Blood Pressure319941822
PubMed | Google Scholar
771 LYNCH, E. C., M. S. BLAKE, E. C. GOTSCHLICH, and A. MAURO. Studies on porins: spontaneously transferred from whole cells and from purified proteins of Neisseria gonorrhoeae and Neisseria meningitidis. Biophys. J. 45: 104–107, 1984.
Google Scholar
772 LYTLE, C., and B. FORBUSH III. The Na-K-Cl cotransport protein of shark rectal gland. II. Regulation by direct phosphorylation. J. Biol. Chem. 267: 25438–25443, 1992.
Google Scholar
773 MA T., FRIGERI A., HASEGAWA H., VERKMAN A. S.Cloning of a water channel homolog expressed in brain meningeal cells and kidney collecting duct that functions as a stilbene-sensitive glycerol transporter.J. Biol. Chem.26919942184521849
Crossref | PubMed | ISI | Google Scholar
774 MACDONALD R. L., ANGELOTTI T. P.Native and recombinant GABA_A receptor channels.Cell. Physiol. Biochem.31993352373
Crossref | ISI | Google Scholar
775 MACKERT B. M., STAUB F., PETERS J., BAETHMANN A., KEMPSKI O.Anoxia in vitro does not induce neuronal swelling or death.J. Neurol. Sci.13919963947
Crossref | PubMed | ISI | Google Scholar
776 MACKNIGHT A. D. C.Principles of cell volume regulation.Renal Physiol. Biochem.111988114141
PubMed | Google Scholar
777 MACKNIGHT A. D. C.The role of anions in cellular volume regulation.Pflügers Arch.405, Suppl.1985S12S16
Crossref | ISI | Google Scholar
778 MACKNIGHT A. D. C., GORDON L. G. M., PURVES R. D.Problems in the understanding of cell volume regulation.J. Exp. Zool.26819948089
Crossref | PubMed | Google Scholar
779 MACKNIGHT A. D. C., LEAF A.Regulation of cellular volume.Physiol. Rev.571977510573
Link | ISI | Google Scholar
780 MACKNIGHT A. D. C., SCOTT R. J.Effects of impermeant medium ions on the composition of rabbit renal cortical slices.Renal Physiol. Biochem.121989118136
PubMed | Google Scholar
781 MACLEAN-FLETCHER S. D., POLLARD T. D.Viscometric analysis of the gelation of Acanthamoeba extracts and purification of two gelation factors.J. Cell Biol.851980414428
Crossref | PubMed | ISI | Google Scholar
782 MACLEOD, R. J. How an epithelial cell swells is a determinant of the signaling pathways that activate RVD. In: Cellular and Molecular Physiology of Cell Volume Regulation, edited by K. Strange. Boca Raton, FL: CRC, 1994, p. 191–200.
Google Scholar
783 MACLEOD R. J., HAMILTON J. R.Activation of Na⁺/H⁺ exchange is required for regulatory volume decrease after modest physiological volume increases in jejunal villus epithelial cells.J. Biol. Chem.27119962313823145
Crossref | PubMed | ISI | Google Scholar
784 MACLEOD R. J., HAMILTON J. R.Separate K⁺ and Cl⁻ transport pathways are activated for regulatory volume decrease in jejunal villus cells.Am. J. Physiol.260(Gastrointest. Liver Physiol. 23)1991G405G415
Google Scholar
785 MACLEOD R. J., HAMILTON J. R.Volume regulation initiated by Na⁺-nutrient cotransport in isolated mammalian villus enterocytes.Am. J. Physiol.260(Gastrointest. Liver Physiol. 23)1991G26G33
Google Scholar
786 MACLEOD R. J., HAMILTON J. R., BATEMAN A., BELCOURT D., HU J., BENNETT H. P., SOLOMON S.Corticostatic peptides cause nifedipine-sensitive volume reduction in jejunal villus enterocytes.Proc. Natl. Acad. Sci. USA881991552556
Crossref | PubMed | ISI | Google Scholar
787 MACLEOD R. J., HAMILTON J. R., KOPELMAN H., SWEEZEY N. B.Developmental differences of cystic fibrosis transmembrane conductance regulator functional expression in isolated rat fetal distal airway epithelial cells.Pediatr. Res.3519944549
Crossref | PubMed | ISI | Google Scholar
788 MACLEOD R. J., LEMBESSIS P., HAMILTON J. R.Differences in Ca²⁺-mediation of hypotonic and Na⁺-nutrient regulatory volume decrease in suspensions of jejunal enterocytes.J. Membr. Biol.13019922331
Crossref | PubMed | ISI | Google Scholar
789 MACROBBIE E. A. C., USSING H. H.Osmotic behaviour of the epithelial cells of frog skin.Acta Physiol. Scand.531961348365
Crossref | PubMed | Google Scholar
790 MADARA J. L., PARKOS C., COLGAN S., MACLEOD R. J., NASH S., MATTHEWS J., DELP C., LENCER W.Cl⁻ secretion in a model intestinal epithelium induced by a neutrophil-derived secretagogue.J. Clin. Invest.89199219381944
Crossref | PubMed | ISI | Google Scholar
791 MAEDA T., WURGLER-MURPHY S. M., SAITO H.A two component system that regulates an osmosensing MAP kinase cascade in yeast.Nature3691994242245
Crossref | PubMed | ISI | Google Scholar
792 MAGER W. H., VARELA J. C.Osmostress response of the yeast Saccharomyces.Mol. Microbiol.101993253258
Crossref | ISI | Google Scholar
793 MAHNENSMITH R. L., ARONSON P. S.The plasma membrane sodium-hydrogen exchanger and its role in physiological and pathophysiological processes.Circ. Res.561985773788
Crossref | PubMed | ISI | Google Scholar
794 MAIRBÄURL H., HOFFMANN J. F.Internal magnesium, 2,3-diphosphoglycerate, and the regulation of the steady-state volume of human red blood cells by the Na/K/2Cl cotransport system.J. Gen. Physiol.991992721746
Crossref | PubMed | ISI | Google Scholar
795 MANARA F. S., CHIN J., SCHNEIDER D. L.Role of degranulation in activation of the respiratory burst in human neutrophils.J. Leukoc. Biol.491991489498
Crossref | PubMed | ISI | Google Scholar
796 MANGANEL M., TURNER R. J.Agonist-induced activation of Na⁺/H⁺ exchange in rat parotid acinar cells is dependent on calcium but not on protein kinase C.J. Biol. Chem.265199042844289
PubMed | ISI | Google Scholar
797 MANGANEL M., TURNER R. J.Rapid secretagogue-induced activation of Na⁺/H⁺ exchange in rat parotid acinar cells. Possible interrelationship between volume regulation and stimulus-secretion coupling.J. Biol. Chem.26619911018210188
PubMed | ISI | Google Scholar
798 MARGALIT A., LIVNE A. A.Lipoxygenase product controls the regulatory volume decrease of human platelets.Platelets21991207214
Crossref | PubMed | Google Scholar
799 MARGALIT A., LIVNE A. A.Human platelets exposed to mechanical stresses express a potent lipoxygenase product.Thromb. Haemostasis681992589594
Crossref | PubMed | ISI | Google Scholar
800 MARGALIT A., LIVNE A. A., FUNDER J., GRANOT Y.Initiation of RVD response in human platelets: mechanical-biochemical transduction involves pertussis-toxin-sensitive G protein and phospholipase A₂ .J. Membr. Biol.1361993303311
Crossref | PubMed | ISI | Google Scholar
801 MARGALIT A., SOFER Y., GROSSMAN S., REYNAUD D., PACE-ASCIAK C. R., LIVNE A. A.Hepoxilin A3 is the endogenous lipid mediator opposing hypotonic swelling of intact human platelets.Proc. Natl. Acad. Sci. USA90199325892592
Crossref | PubMed | ISI | Google Scholar
802 MARTIN D. L., SHAIN W.Beta-adrenergic-agonist stimulated taurine release from astroglial cells is modulated by extracellular [K⁺] and osmolarity.Neurochem. Res.181993437444
Crossref | PubMed | ISI | Google Scholar
803 MARTINEZ-MALDONADO, M., J. E. BENABE, and H. R. CORDOVA. Chronic clinical intrinsic renal failure. In: The Kidney: Physiology and Pathophysiology (2nd ed.), edited by D. W. Seldin and G. Giebisch. New York: Raven, 1992, p. 3227–3288.
Google Scholar
804 MARTINS E. A., MENEGHINI R.Cellular DNA damage by hydrogen peroxide is attenuated by hypotonicity.Biochem. J.2991994137140
Crossref | PubMed | ISI | Google Scholar
805 MARUNAKA Y., SHINTANI Y., SUGIMOTO E., NIISATO N.Roles of the tyrosine kinase in insulin action on cell volume of fetal rat type II pneumocytes.Pflügers Arch.4321996571573
Crossref | PubMed | ISI | Google Scholar
806 MARX G., BLANKENFELD A., PANET R., GORODETSKY R.Model for the regulation of platelet volume and responsiveness by the transmembrane Na⁺/K⁺-pump.J. Cell. Physiol.1511992249254
Crossref | PubMed | ISI | Google Scholar
807 MASHINO T., FRIDOVICH I.Effects of urea and trimethylamine-N-oxide on enzyme activity and stability.Arch. Biochem. Biophys.2581987356360
Crossref | PubMed | ISI | Google Scholar
808 MASTROCOLA T., LAMBERT I. H., KRAMHØFT B., RUGOLO M., HOFFMANN E. K.Volume regulation in human fibroblasts: role of Ca²⁺ and 5-lipoxygenase products in the activation of the Cl⁻ efflux.J. Membr. Biol.13619935562
Crossref | PubMed | ISI | Google Scholar
809 MATSUDA, S., H. KAWASAKI, T. MORIGUCHI, Y. GOTOH, and E. NISHIDA. Activation of protein kinase cascades by osmotic shock. J. Biol. Chem.: 270: 12781–12786, 1995.
Google Scholar
810 MATSUMOTO T., VAN DER AUWERA P., WATANABE Y., TANAKA M., OGATA N., NAITO S., KUMAZAWA J.Neutrophil function in hyperosmotic NaCl is preserved by phosphoenolpyruvate.Urol. Res.191991223227
Crossref | PubMed | Google Scholar
811 MATTHEWS C. C., FELDMAN E. L.Insulin-like growth factor I rescues SH-SY5Y human neuroblastoma cells from hyperosmotic induced programmed cell death.J. Cell. Physiol.1661996323331
Crossref | PubMed | ISI | Google Scholar
812 MATTHEWS, J. B., C. S. AWTREY, and J. L. MADARA. Microfilament-dependent activation of Na⁺/K⁺/2Cl⁻ cotransport by cAMP in intestinal epithelial monolayers. J. Clin. Invest. 90: 1608–1613, 1992 (published erratum appears in J. Clin. Invest. 91: 1855, 1993).
Google Scholar
813 MATTHEWS J. B., SMITH J. A., HRNJEZ B. J.Effects of F-actin stabilization or disassembly on epithelial Cl secretion and Na-K-2Cl cotransport.Am. J. Physiol.272(Cell Physiol. 41)1997C254C262
Link | Google Scholar
814 MATTHEWS J. B., SMITH J. A., TALLY K. J., AWTREY C. S., NGUYEN H., RICH J., MADARA J. L.Na-K-2Cl cotransport in intestinal epithelial cells. Influence of chloride efflux and F-actin on regulation of cotransporter activity and bumetanide binding.J. Biol. Chem.26919941570315709
PubMed | ISI | Google Scholar
815 McCARTY N. A., O'NEIL R. G.Calcium signaling in cell volume regulation.Physiol. Rev.72199210371061
Link | ISI | Google Scholar
816 McMANUS, M. L., and K. B. CHURCHWELL. Clinical significance of cellular osmoregulation. In: Cellular and Molecular Physiology of Cell Volume Regulation, edited by K. Strange. Boca Raton, FL: CRC, 1994, p. 63–77.
Google Scholar
817 McMANUS M. L., CHURCHWELL K. B., STRANGE K.Regulation of cell volume in health and disease.N. Engl. J. Med.333199512601266
Crossref | PubMed | ISI | Google Scholar
818 McMANUS M. L., SERHAN C., JACKSON P., STRANGE K.Ketoconazole blocks organic osmolyte efflux independently of its effect on arachidonic acid conversion.Am. J. Physiol.267(Cell Physiol. 36)1994C266C271
Link | Google Scholar
819 MEIJER A. J., BAQUET A., GUSTAFSON L., VAN WOERKOM G. M., HUE L.Mechanism of activation of liver glycogen synthase by swelling.J. Biol. Chem.267199258235828
PubMed | ISI | Google Scholar
820 MEIJER A. J., GUSTAFSON L. A., LUIKEN J. J. F. P., BLOMMAART P. J. E., CARO L. H. P., VAN WOERKOM G. M., SPRONK C., BOON L.Cell swelling and the sensitivity of autophagic proteolysis to inhibition by amino acids in isolated rat hepatocytes.Eur. J. Biochem.2151993449454
Crossref | PubMed | Google Scholar
821 MELMED R. N., KARANIAN P. J., BERLIN R. D.Control of cell volume in the J774 macrophage by microtubule disassembly and cyclic AMP.J. Cell Biol.901981761768
Crossref | PubMed | ISI | Google Scholar
822 MELTON J. E., PATLAK C. S., PETTIGREW K. D., CSERR H. F.Volume regulatory loss of Na⁺, Cl⁻, and K⁺ from rat brain during acute hyponatremia.Am. J. Physiol.252(Renal Fluid Electrolyte Physiol. 21)1987F661F669
Google Scholar
823 Meng, X. J., and S. A. Weinman. cAMP- and swelling-activated chloride conductance in rat hepatocytes. Am. J. Physiol. 271 (Cell Physiol. 40): C112–C120, 1996.
Google Scholar
824 MEYER M., MALY K., UBERALL F., HOFLACHER J., GRUNICKE H.Stimulation of K⁺ transport systems by Ha-ras.J. Biol. Chem.266199182308235
PubMed | ISI | Google Scholar
825 MILLAR I. D., BARBER M. C., LOMAX M. A., TRAVERS M. T., SHENNAN D. B.Mammary protein synthesis is acutely regulated by the cellular hydration state.Biochem. Biophys. Res. Commun.2301997351355
Crossref | PubMed | ISI | Google Scholar
826 MILLER R. T., COUNILLON L., PAGES G., LIFTON R. P., SARDET C., POUYSSEGUR J.Structure of the 5′-flanking regulatory region and gene for the human growth factor-activatable Na/H exchanger NHE-1.J. Biol. Chem.26619911081310819
PubMed | ISI | Google Scholar
827 MILLS G. B., CRAGOE E. J.Jr., E. W. GELFAND, and S. GRINSTEIN. Interleukin 2 induces a rapid increase in intracellular pH through activation of a Na⁺/H⁺ antiport.J. Biol. Chem.26019851250012507
PubMed | ISI | Google Scholar
828 MILLS J. W.The cell cytoskeleton: possible role in volume control.Curr. Top. Membr. Transp.30198775101
Crossref | ISI | Google Scholar
829 MILLS J. W., LUBIN M.Effect of adenosine 3′,5′-cyclic monophosphate on volume and cytoskeleton of MDCK cells.Am. J. Physiol.250(Cell Physiol. 19)1986C319C324
Link | Google Scholar
830 MILLS J. W., SCHWIEBERT E. M., STANTON B. A.Evidence for the role of actin filaments in regulating cell swelling.J. Exp. Zool.2681994111120
Crossref | PubMed | Google Scholar
831 MILLS, J. W., E. M. SCHWIEBERT, and B. A. STANTON. The cytoskeleton and cell volume regulation. In: Cellular and Molecular Physiology of Cell Volume Regulation, edited by K. Strange. Boca Raton, FL: CRC, 1994, p. 241–258.
Google Scholar
832 MILLS J. W., SCHWIEBERT E. M., STANTON B. A.The cytoskeleton and membrane transport.Curr. Opin. Nephrol. Hypertens.31994529534
Crossref | PubMed | Google Scholar
833 MILLS J. W., SKIEST D. L.Role of cyclic AMP and the cytoskeleton in volume control in MDCK cells.Mol. Physiol.81985247262
Google Scholar
834 MINTON A. P.Excluded volume as a determinant of macromolecular structure and reactivity.Biopolymers20198120932120
Crossref | ISI | Google Scholar
835 MINTON, A. P. Influence of macromolecular crowding on intracellular association reactions: possible role in volume regulation. In: Cellular and Molecular Physiology of Cell Volume Regulation, edited by K. Strange. Boca Raton, FL: CRC, 1994, p. 181–190.
Google Scholar
836 MINTON A. P.Macromolecular crowding and molecular recognition.J. Mol. Recognit.61993211214
Crossref | PubMed | Google Scholar
837 MINTON A. P.The effect of volume occupancy upon the thermodynamic activity of proteins: some biochemical consequences.Mol. Cell. Biochem.551983119140
Crossref | PubMed | ISI | Google Scholar
838 MINTON A. P., COLCLASURE G. C., PARKER J. C.Model for the role of macromolecular crowding in regulation of cellular volume.Proc. Natl. Acad. Sci. USA8919921050410506
Crossref | PubMed | ISI | Google Scholar
839 MISGELD U., DEISZ R. A., DODT H. U., LUX H. D.The role of chloride transport in postsynaptic inhibition of hippocampal neurons.Science232198614131415
Crossref | PubMed | ISI | Google Scholar
840 MIYOSHI K., FUNAHASHI H., OKUDA K., NIWA K.Development of rat one-cell embryos in a chemically defined medium: effects of glucose, phosphate and osmolarity.J. Reprod. Fertil.10019942126
Crossref | PubMed | Google Scholar
841 MOIR A. M., ZAMMIT V. A.Insulin-independent and extremely rapid switch in the partitioning of hepatic fatty acids from oxidation to esterification in starved-refed diabetic rats. Possible roles for changes in cell pH and volume.Biochem. J.3051995953958
Crossref | PubMed | ISI | Google Scholar
842 MOLSKI T. F., NACCACHE P. H., BORGEAT P., SHA'AFI R. I.Similarities in the mechanisms by which formyl-methionyl-leucyl-phenylalanine, arachidonic acid, and leukotriene B₄ increase calcium and sodium influxes in rabbit neutrophils.Biochem. Biophys. Res. Commun.1031981227232
Crossref | PubMed | ISI | Google Scholar
843 MONTROSE-RAFIZADEH C., GUGGINO W. B.Cell volume regulation in the nephron.Annu. Rev. Physiol.521990761772
Crossref | PubMed | ISI | Google Scholar
844 MOOLENAAR W. H.Effects of growth factors on intracellular pH regulation.Annu. Rev. Physiol.481986363376
Crossref | PubMed | ISI | Google Scholar
845 MOORMAN J. R., ACKERMAN S. J., KOWDLEY G. C., GRIFFIN M. P., MOUNSEY J. P., CHEN Z., CALA S. E., O'BRIEN J. J., SZABO G., JONES L. R.Unitary anion currents through phospholemman channel molecules.Nature3771995737740
Crossref | PubMed | ISI | Google Scholar
846 MORAN A., TURNER R. J.Secretagogue-induced RVD in HSY cells is due to K⁺ channels activated by Ca²⁺ and protein kinase C.Am. J. Physiol.265(Cell Physiol. 34)1993C1405C1411
Link | Google Scholar
847 MORAN J., HURTADO S., PASANTES H.MORALES. Similar properties of taurine release induced by potassium and hyposmolarity in the rat retina.Exp. Eye Res.531991347352
Crossref | PubMed | ISI | Google Scholar
848 MORAN J., SABANERO M., MEZA I., PASANTES-MORALES H.Changes of actin cytoskeleton during swelling and regulatory volume decrease in cultured astrocytes.Am. J. Physiol.271(Cell Physiol. 40)1996C1901C1907
Link | Google Scholar
849 MORATINOS J., REVERTE M.Effects of catecholamines on plasma potassium: the role of alpha and beta adrenoceptors.Fundam. Clin. Pharmacol.71993143153
Crossref | PubMed | ISI | Google Scholar
850 MORETTI R., MARTIN M., PROVERBIO T., PROVERBIO F., MARIN R.Ouabain-insensitive Na-ATPase activity in homogenates from different animal tissues.Comp. Biochem. Physiol.981991623626
Google Scholar
851 MORGAN H. E., XENOPHONTOS X. P., HANEDA T., McGLAUGHIN S., WATSON P. A.Stretch-anabolism transduction.J. Appl. Cardiol.41989415422
Google Scholar
852 MORGAN J. M.Osmoregulation and water stress in higher plants.Annu. Rev. Plant Physiol.351984299319
Crossref | Google Scholar
853 MORIGUCHI T., KAWASAKI H., MATSUDA S., GOTOH Y., NISHIDA E.Evidence for multiple activators for stress-activated protein kinase/c-Jun amino-terminal kinases. Existence of novel activators.J. Biol. Chem.27019951296912972
Crossref | PubMed | ISI | Google Scholar
854 MORIYAMA T., GARCIA-PÉREZ A., BURG M. B.Osmotic regulation of aldose reductase protein synthesis in renal medullary cells.J. Biol. Chem.26419891681016814
PubMed | ISI | Google Scholar
855 MORIYAMA T., GARCIA-PÉREZ A., BURG M. B.Factors affecting the ratio of different organic osmolytes in renal medullary cells.Am. J. Physiol.259(Renal Fluid Electrolyte Physiol. 28)1990F847F858
Google Scholar
856 MORIYAMA T., MURPHY H. R., MARTIN B. M., GARCIA-PÉREZ A.Detection of specific mRNAs in single nephron segments by use of the polymerase chain reaction.Am. J. Physiol.258(Renal Fluid Electrolyte Physiol. 27)1990F1470F1474
Google Scholar
857 MORRIS C. E.Mechanosensitive ion channels.J. Membr. Biol.113199093107
Crossref | PubMed | ISI | Google Scholar
858 MORRIS-JONES P. H., HOUSTON I. B., EVANS R. C.Prognosis of the neurological complications of acute hypernatremia.Lancet2196713851389
Crossref | PubMed | ISI | Google Scholar
859 MORTIMORE G. E., PÖSÖ A. R.Intracellular protein catabolism and its control during nutrient deprivation and supply.Annu. Rev. Nutr.71987539564
Crossref | PubMed | ISI | Google Scholar
860 MORTIMORE G. E., PÖSÖ A. R.Lysosomal pathways in hepatic protein degradation: regulatory role of amino acids.Federation Proc.43198412891294
PubMed | Google Scholar
861 MOTAIS R., FIEVET B., BORGESE F., GARCIA-ROMEU F.Association of the band 3 protein with a volume activated anion and amino acid channel, a molecular approach.J. Exp. Biol.2001997361367
PubMed | ISI | Google Scholar
862 MOTAIS R., GUIZOUARN H., GARCIA-ROMEU F.Red cell volume regulation: the pivotal role of ionic strength in controlling swelling-dependent transport systems.Biochim. Biophys. Acta10751991169180
Crossref | PubMed | ISI | Google Scholar
863 MOYES, C. D., and T. W. MOON. Solute effects on the glycine cleavage system of two osmoconformers Raja erinacea and Mya arenaria and an osmoregulator Pseudopleuronectes americanus. J. Exp. Zool. 242: 1–8, 1987.
Google Scholar
864 MUALLEM S., ZHANG B. X., LOESSBERG P. A., STAR R. A.Simultaneous recording of cell volume changes and intracellular pH or Ca²⁺ concentration in single osteosarcoma cells UMR-106–01.J. Biol. Chem.26719921765817664
PubMed | ISI | Google Scholar
865 MÜLLER D.Long-term potentiation and glutamate receptors: a role for protein kinases.Renal Physiol. Biochem.171994157160
PubMed | Google Scholar
866 MURPHY D., CARTER D.Vasopressin gene expression in the rodent hypothalamus: transcriptional and posttranscriptional responses to physiological stimulation.Mol. Endocrinol.4199010511059
Crossref | PubMed | Google Scholar
867 MURPHY M. G., JOLLIMORE C., CROCKER J. F., HER H.Beta-oxidation of [1-¹⁴C]palmitic acid by mouse astrocytes in primary culture: effects of agents implicated in the encephalopathy of Reye's syndrome.J. Neurosci. Res.331992445454
Crossref | PubMed | ISI | Google Scholar
868 MUSCH M. W., GOLDSTEIN L.High affinity binding of ankyrin induced by volume expansion in skate erythrocytes.J. Biol. Chem.27119962122121225
Crossref | PubMed | ISI | Google Scholar
869 MUSCH M. W., LEFFINGWELL T. R., GOLDSTEIN L.Band 3 modulation and hypotonic-stimulated taurine efflux in skate erythrocytes.Am. J. Physiol.266(Regulatory Integrative Comp. Physiol. 35)1994R65R74
Google Scholar
870 NACCACHE P. H., SHOWELL H. J., BECKER E. L., SHA'AFI R. I.Transport of sodium, potassium, and calcium across rabbit polymorphonuclear leukocyte membranes: effect of chemotactic factor.J. Cell Biol.731977428444
Crossref | PubMed | ISI | Google Scholar
871 NACCACHE P. H., SHOWELL H. J., BECKER E. L., SHA'AFI R. I.Changes in ionic movements across rabbit polymorphonuclear leukocyte membranes during lysosomal enzyme release. Possible ionic basis for lysosomal enzyme release.J. Cell Biol.751977635649
Crossref | PubMed | ISI | Google Scholar
872 NAKAHARI T., MURAKAMI M., SASAKI Y., KATAOKA T., IMAI Y., SHIBA Y., KANNO Y.Dose effects of acetylcholine on the cell volume of rat mandibular salivary acini.Jpn. J. Physiol.411991153168
Crossref | PubMed | Google Scholar
873 NAKAHARI T., MURAKAMI M., YOSHIDA H., MIYAMOTO M., SOHMA Y., IMAI Y.Decrease in rat submandibular acinar cell volume during ACh stimulation.Am. J. Physiol.258(Gastrointest. Liver Physiol. 21)1990G878G886
Google Scholar
874 NAKAHARI T., STEWARD M. C., YOSHIDA H., IMAI Y.Osmotic flow transients during acetylcholine stimulation in the perfused rat submandibular gland.Exp. Physiol.8219975570
Crossref | PubMed | ISI | Google Scholar
875 NAKANISHI T., BALABAN R. S., BURG M. B.Survey of osmolytes in renal cell lines.Am. J. Physiol.255(Cell Physiol. 24)1988C181C191
Link | Google Scholar
876 NAKANISHI T., BURG M. B.Osmoregulatory fluxes of myo-inositol and betaine in renal cells.Am. J. Physiol.257(Cell Physiol. 26)1989C964C970
Link | Google Scholar
877 NAKANISHI T., TURNER R. J., BURG M. B.Osmoregulatory changes in myo-inositol transport by renal cells.Proc. Natl. Acad. Sci. USA86198960026006
Crossref | PubMed | ISI | Google Scholar
878 NAKANISHI T., TURNER R. J., BURG M. B.Osmoregulation of betaine transport in mammalian renal medullary cells.Am. J. Physiol.258(Renal Fluid Electrolyte Physiol. 27)1990F1061F1067
Google Scholar
879 NAKANISHI T., UYAMA O., NAKAHAMA H., TAKAMITSU Y., SUGITA M.Determinants of relative amounts of medullary organic osmolytes: effects of NaCl and urea differ.Am. J. Physiol.264(Renal Fluid Electrolyte Physiol. 33)1993F472F479
Google Scholar
880 NAKANISHI T., YAMAUCHI A., NAKAHAMA H., YAMAMURA Y., YAMADA Y., ORITA Y., FUJIWARA Y., UYEDA N., TAKAMITSU Y., SUGITA M.Organic osmolytes in rat renal inner medulla are modulated by vasopressin V₁ and/or V₂ antagonists.Am. J. Physiol.267(Renal Fluid Electrolyte Physiol. 36)1994F146F152
Google Scholar
881 NATARAJAN R., GONZALES N., XU L., NADLER J. L.Vascular smooth muscle cells exhibit increased growth in response to elevated glucose.Biochem. Biophys. Res. Commun.1871992552560
Crossref | PubMed | ISI | Google Scholar
882 NAUNTOFTE B.Regulation of electrolyte and fluid secretion in salivary acinar cells.Am. J. Physiol.263(Gastrointest. Liver Physiol. 26)1992G823G837
Google Scholar
883 NEARY J. T., FU Q., BENDER A. S., NORENBERG M. D.Effect of external acidosis on basal and ATP-evoked calcium influx in cultured astrocytes.Brain Res.6041993211216
Crossref | PubMed | ISI | Google Scholar
884 NEEDHAM D.Possible role of cell cycle-dependent morphology, geometry, and mechanical properties in tumor cell metastasis.Cell. Biophys.18199199121
Crossref | PubMed | Google Scholar
885 NEGULESCU P. A., MUNCK B., MACHEN T. E.Volume-sensitive Ca influx and release from intracellular pools in gastric parietal cells.Am. J. Physiol.263(Cell Physiol. 32)1992C584C589
Link | Google Scholar
886 NEWSOME W. P., WARSKULAT U., NOE B., WETTSTEIN M., STOLL B., GEROK W., HÄUSSINGER D.Modulation of phosphoenolpyruvate carboxykinase mRNA levels by the hepatocellular hydration state.Biochem. J.3041994555560
Crossref | PubMed | ISI | Google Scholar
887 NG L. L., DUDLEY C., BOMFORD J., HAWLEY D.Leukocyte intracellular pH and Na⁺/H⁺ antiport activity in human hypertension.J. Hypertens.71989471475
Crossref | PubMed | ISI | Google Scholar
888 NG L. L., SIMMONS D., FRIGHI V., GARRIDO M. C., BOMFORD J.Effect of protein kinase C modulators on the leucocyte Na⁺/H⁺ antiport in type 1 (insulin-dependent) diabetic subjects with albuminuria.Diabetologia331990278284
Crossref | PubMed | ISI | Google Scholar
889 NG L. L., SIMMONS D., FRIGHI V., GARRIDO M. C., BOMFORD J., HOCKADAY T. D. R.Leukocyte Na⁺/H⁺ antiport activity in type 1 (insulin-dependent) diabetic patients with nephropathy.Diabetologia331990371377
Crossref | PubMed | ISI | Google Scholar
890 NGEZAHAYO A., KOLB H.-A.Gap junctional permeability is affected by cell volume changes and modulates volume regulation.FEBS Lett.276199068
Crossref | PubMed | ISI | Google Scholar
891 NICOLL R. A., MALENKA R. C., KAUER J. A.Functional comparison of neurotransmitter receptor subtypes in mammalian central nervous system.Physiol. Rev.701990514565
Link | ISI | Google Scholar
892 NIELSEN B. W., BJERKE T., DAMSGAARD T. M., HERLIN T., THESTRUP-PEDERSEN K., SCHIOTZ P. O.Hyperosmolarity selectively enhances IgE-receptor-mediated histamine release from human basophils.Agents Actions351992170178
Crossref | PubMed | Google Scholar
893 NILIUS B., WOHLRAB W.Potassium channels and regulation of proliferation of human melanoma cells.J. Physiol. (Lond.)4451992537548
Crossref | Google Scholar
894 NISHINA H., FISCHER K. D., RADVANYI L., SHAHINIAN A., HAKEM R., RUBIE E. A., BERNSTEIN A., MAK T. W., WOODGETT J. R., PENNINGER J. M.Stress signalling kinase Sek1 protects thymocytes from apoptosis mediated by CD95 and CD3.Nature3851997350353
Crossref | PubMed | ISI | Google Scholar
895 NOE B., SCHLIESS F., WETTSTEIN M., HEINRICH S., HÄUSSINGER D.Regulation of taurocholate excretion by a hypoosmolarity-activated signal transduction pathway in rat liver.Gastroenterology1101996858865
Crossref | PubMed | ISI | Google Scholar
896 NORENBERG M. D.Astrocyte responses to CNS injury.J. Neuropathol. Exp. Neurol.531994213220
Crossref | PubMed | ISI | Google Scholar
897 NORENBERG M. D., BAKER L., NORENBERG L. O., BLICHARSKA J., BRUCE-GREGORIOS J. H., NEARY J. T.Ammonia-induced astrocyte swelling in primary culture.Neurochem. Res.161991833836
Crossref | PubMed | ISI | Google Scholar
898 NORENBERG M. D., BENDER A. S.Astrocyte swelling in liver failure: role of glutamine and benzodiazepines.Acta Neurochir.6019942427
Google Scholar
899 NORRIE D. H., WOLSTENHOLME J., HOWCROFT H., STEPHEN J.Vaccinia virus-induced changes in [Na⁺] and [K⁺] in HeLa cells.J. Gen. Virol.621982127136
Crossref | PubMed | ISI | Google Scholar
900 OBERLEITHNER H., GIEBISCH G., LANG F., WANG W.Cellular mechanism of the furosemide sensitive transport system in the kidney.Klin. Wochenschr.60198211731179
Crossref | PubMed | Google Scholar
901 O'BRIEN J. A., WALTERS R. J., VALVERDE M. A., SEPULVEDA F. V.Regulatory volume increase after hypertonicity- or vasoactive-intestinal-peptide-induced cell-volume decrease in small-intestinal crypts is dependent on Na⁺-K⁺-2Cl⁻ cotransport.Pflügers Arch.42319936773
Crossref | PubMed | ISI | Google Scholar
902 O'CONNOR E. R., KIMELBERG H. K., KEESE C. R., GIAEVER I.Electrical resistance method for measuring volume changes in monolayer cultures applied to primary astrocyte cultures.Am. J. Physiol.264(Cell Physiol. 33)1993C471C478
Link | Google Scholar
903 O'DONNELL M. E., MARTINEZ A., SUN D.Endothelial Na-K-Cl cotransport regulation by tonicity and hormones: phosphorylation of cotransport protein.Am. J. Physiol.269(Cell Physiol. 38)1995C1513C1523
Link | Google Scholar
904 OFFENSPERGER W. B., OFFENSPERGER S., STOLL B., GEROK W., HÄUSSINGER D.Effects of anisotonic exposure on duck hepatitis B virus replication.Hepatology20199417
PubMed | ISI | Google Scholar
905 OH M. S., CARROLL H. J.Disorders of sodium metabolism: hypernatremia and hyponatremia.Crit. Care Med.20199294103
Crossref | PubMed | ISI | Google Scholar
906 OHNISHI S., HARA M., INAGAKI C., YAMASHITA T., KUMAZAWA T.Regulation of Cl⁻ conductance in delayed shortening and shrinkage of outer hair cells.Acta Otolaryngol. Suppl.50019934245
Crossref | PubMed | Google Scholar
907 OHTSUYAMA M., SUZUKI Y., SAMMAN G., SATO F., SATO K.Cell volume analysis of gramicidin-treated eccrine clear cells to study regulation of Cl channels.Am. J. Physiol.265(Cell Physiol. 34)1993C1090C1099
Link | Google Scholar
908 OIKI S., KUBO M., OKADA Y.Mg²⁺ and ATP-dependence of volume-sensitive Cl⁻ channels in human epithelial cells.Jpn. J. Physiol.44, Suppl.1994S77S79
Google Scholar
909 OKA J. A., CHRISTENSEN M. D., WEIGEL P. H.Hyperosmolarity inhibits galactosyl receptor-mediated but not fluid phase endocytosis in isolated rat hepatocytes.J. Biol. Chem.26419891201612024
PubMed | ISI | Google Scholar
910 OKADA H., ISHII K., NUNOKI K., TAIRA N.Cloning of a swelling-induced chloride current related protein from rabbit heart.Biochim. Biophys. Acta12341995145148
Crossref | PubMed | ISI | Google Scholar
911 OKADA M., SAITO Y., SAWADA E., NISHIYAMA A.Microfluorimetric imaging study of the mechanism of activation of the Na⁺/H⁺ antiport by muscarinic agonist in rat mandibular acinar cells.Pflügers Arch.4191991338348
Crossref | PubMed | ISI | Google Scholar
911a OKADA Y.Volume expansion-sensing outward-rectifier Cl⁻ channel: fresh start to the molecular identity and volume sensor.Am. J. Physiol.273(Cell Physiol. 42)1997C755C789
Link | Google Scholar
912 OKADA Y., HAZAMA A., HASHIMOTO A., MARUYAMA Y., KUBO M.Exocytosis upon osmotic swelling in human epithelial cells.Biochim. Biophys. Acta11071992201205
Crossref | PubMed | ISI | Google Scholar
913 OLIET S. H., BOURQUE C. W.Mechanosensitive channels transduce osmosensitivity in supraoptic neurons.Nature3641993341343
Crossref | PubMed | ISI | Google Scholar
914 OLIVIERI O., VITOUX D., GALACTEROS F., BACHIR D., BLOUQUIT Y., BEUZARD Y., BRUGNARA C.Hemoglobin variants and activity of the (K⁺Cl⁻) cotransport system in human erythrocytes.Blood791992793797
Crossref | PubMed | ISI | Google Scholar
915 OLSON J. E., EVERS J. A., BANKS M.Brain osmolyte content and blood-brain barrier water permeability surface area product in osmotic edema.Acta Neurochir. Suppl.601994571573
PubMed | Google Scholar
916 O'NEILL W. C., STEINBERG D. F.Functional coupling of Na⁺-K⁺-2Cl⁻ cotransport and Ca²⁺-dependent K⁺ channels in vascular endothelial cells.Am. J. Physiol.269(Cell Physiol. 38)1995C267274
Link | Google Scholar
917 ORDWAY R. W., PETROU S., KIRBER M. T.Jr., J. V. WALSH, and J. J. SINGER. Two distinct mechanisms of ion channel activation by membrane stretch: evidence that endogenous fatty acids mediate stretch activation of K⁺ channels (Abstract).Biophys. J.611992A391
Google Scholar
918 ORFALI K. A., SUGDEN M. C.Interactive effects of alpha-adrenergic agonists and increased cell volume on deoxyglucose uptake and phosphorylation in isolated ventricular myocytes (Abstract).Biochem. Soc. Trans.221994162S
Crossref | PubMed | ISI | Google Scholar
919 ORLOV S. N., RESINK T. J., BERNHARDT J., BUHLER F. R.Volume-dependent regulation of sodium and potassium fluxes in cultured vascular smooth muscle cells: dependence on medium osmolality and regulation by signalling systems.J. Membr. Biol.1291992199210
Crossref | PubMed | ISI | Google Scholar
920 ORRINGER E. P., BROCKENBROUGH J. S., WHITNEY J. A., GLOSSON P. S., PARKER J. C.Okadaic acid inhibits activation of K-Cl cotransport in red blood cells containing hemoglobins S and C.Am. J. Physiol.261(Cell Physiol. 30)1991C591C593
Link | Google Scholar
921 OSEHOBO E. P., ANDREW R. D.Osmotic effects upon the theta rhythm, a natural brain oscillation in the hippocampal slice.Exp. Neurol.1241993192199
Crossref | PubMed | ISI | Google Scholar
922 OSHIMI Y., MIYAZAKI S.Fas antigen-mediated DNA fragmentation and apoptotic morphologic changes are regulated by elevated cytosolic Ca²⁺ level.J. Immunol.1541995599609
PubMed | ISI | Google Scholar
923 OSSWALD, H., and U. QUAST. Ion channels and renin secretion from juxtaglomerular cells. In: The Electrophysiology of Neuroendocrine Cells, edited by H. Scherübl and J. Hescheler. Boca Raton, FL: CRC, 1995, p. 301–314.
Google Scholar
924 OUAHBI A., DUCHENE C., GILLES R.Comparative studies of volume restoration following cold-stress induced swelling in renal tissues. I. Effects of ouabain, K⁺ free medium, colchicine and cytochalasin B on rat and rabbit kidney cortex slices.Comp. Biochem. Physiol. A Physiol.971990265273
Crossref | ISI | Google Scholar
925 PAGLIACCI M. C., SPINOZZI F., MIGLIORATI G., FUMI G., SMACCHIA M., GRIGNANI F., RICCARDI C., NICOLETTI I.Genistein inhibits tumour cell growth in vitro but enhances mitochondrial reduction of tetrazolium salts: a further pitfall in the use of the MTT assay for evaluating cell growth and survival.Eur. J. Cancer29199315731577
Crossref | ISI | Google Scholar
926 PALEG L. G., DOUGLAS T. J., VAN DAAL A., KEECH D. B.Proline, betaine and other organic solutes protect enzymes against heat inactivation.Aust. J. Plant Physiol.81981107114
Google Scholar
927 PALFREY, H. C. Protein phosphorylation control in the activity of volume-sensitive transport systems. In: Cellular and Molecular Physiology of Cell Volume Regulation, edited by K. Strange. Boca Raton, FL: CRC, 1994, p. 201–214.
Google Scholar
928 PALFREY H. C., O'DONNELL M. E.Characteristics and regulation of the Na/K/2Cl cotransporter.Cell. Physiol. Biochem.21992293307
Crossref | Google Scholar
929 PAOLETTI P., ASCHER P.Mechanosensitivity of NMDA receptors in cultured mouse central neurons.Neuron131994645655
Crossref | PubMed | ISI | Google Scholar
930 PAPPENHEIMER J. R., VOLPP K.Transmucosal impedance of small intestine: correlation with transport of sugars and amino acids.Am. J. Physiol.263(Cell Physiol. 32)1992C480C493
Link | Google Scholar
931 PARCZYK K., KONDOR-KOCH C.The influence of pH on the vesicular traffic to the surface of the polarized epithelial cell, MDCK.Eur. J. Cell Biol.481989353359
PubMed | ISI | Google Scholar
932 PARKER J. C.Sodium and calcium movements in dog red blood cells.J. Gen. Physiol.711978117
Crossref | PubMed | ISI | Google Scholar
933 PARKER J. C.Volume-responsive sodium movements in dog red blood cells.Am. J. Physiol.244(Cell Physiol. 13)1983C324C330
Link | Google Scholar
934 PARKER J. C.Glutaraldehyde fixation of sodium transport in dog red blood cells.J. Gen. Physiol.841984789803
Crossref | PubMed | ISI | Google Scholar
935 PARKER J. C.Interactions of lithium and protons with the sodium-proton exchanger of dog red blood cells.J. Gen. Physiol.871986189200
Crossref | PubMed | ISI | Google Scholar
936 PARKER J. C.Urea alters set point volume for K-Cl cotransport, Na-H exchange, and Ca-Na exchange in dog red blood cells.Am. J. Physiol.265(Cell Physiol. 34)1993C447C452
Link | Google Scholar
937 PARKER, J. C. In defense of cell volume? Am. J. Physiol. 265 (Cell Physiol. 34): C1191–C1200, 1993.
Google Scholar
938 PARKER, J. C. Coordinated regulation of volume-activated transport pathways. In: Cellular and Molecular Physiology of Cell Volume Regulation, edited by K. Strange. Boca Raton, FL: CRC, 1994, p. 311–324.
Google Scholar
939 PARKER J. C., COLCLASURE G. C.Actions of thiocyanate and N-phenylmaleimide on volume-responsive Na and K transport in dog red cells.Am. J. Physiol.262(Cell Physiol. 31)1992C418C421
Link | Google Scholar
940 PARKER J. C., COLCLASURE G. C.Macromolecular crowding and volume perception in dog red cells.Mol. Cell. Biochem.1141992911
Crossref | PubMed | ISI | Google Scholar
941 PARKER J. C., COLCLASURE G. C., McMANUS T. J.Coordinated regulation of shrinkage-induced Na/H exchange and swelling-induced [K-Cl] cotransport in dog red cells. Further evidence from activation kinetics and phosphatase inhibition.J. Gen. Physiol.981991869880
Crossref | PubMed | ISI | Google Scholar
942 PARKER J. C., DUNHAM P. B., MINTON A. P.Effects of ionic strength on the regulation of Na/H exchange and K-Cl cotransport in dog red blood cells.J. Gen. Physiol.1051995677699
Crossref | PubMed | ISI | Google Scholar
943 PARKER J. C., GITELMAN H. J., McMANUS T. J.Role of Mg in the activation of Na-H exchange in dog red cells.Am. J. Physiol.257(Cell Physiol. 26)1989C1038C1041
Link | Google Scholar
944 PARKER J. C., McMANUS T. J., STARKE L. C., GITELMAN H. J.Coordinated regulation of Na/H exchange and [K-Cl] cotransport in dog red cells.J. Gen. Physiol.96199011411152
Crossref | PubMed | ISI | Google Scholar
945 PARRY-BILLINGS M., BEVAN S. J., OPARA E., NEWSHOLME E. A.Effects of changes in cell volume on the rates of glutamine and alanine release from rat skeletal muscle in vitro.Biochem. J.2761991559561
Crossref | PubMed | ISI | Google Scholar
946 PARSONS D. F.Tumor cell interactions with stromal elastin and type I collagen: the consequences of specific adhesion and proteolysis.Tumor Biol.141993137143
Crossref | PubMed | Google Scholar
947 PAULMICHL M., FRIEDRICH F., MALY K., LANG F.The effect of hyposmolarity on the electrical properties of Madin-Darby canine kidney cells.Pflügers Arch.4131989456462
Crossref | PubMed | ISI | Google Scholar
948 PAULMICHL M., GSCHWENTNER M., WÖLL E., SCHMARDA A., RITTER M., KANIN G., ELLEMUNTER H., WAITZ W., DEETJEN P.Insight into the structure-function relation of chloride channels.Cell. Physiol. Biochem.31993374387
Crossref | ISI | Google Scholar
949 PAULMICHL M., LI Y., WICKMAN K., ACKERMAN M., PERALTA E., CLAPHAM D.New mammalian chloride channel identified by expression cloning.Nature3561992238241
Crossref | PubMed | ISI | Google Scholar
950 PAULMICHL M., WÖLL E., WEISS H., WALDEGGER S., LANG F.Effect of trifluoperazine on renal epitheloid Madin-Darby canine kidney cells.J. Cell. Physiol.1481991314319
Crossref | PubMed | ISI | Google Scholar
951 PAYNE, J. A., and B. FORBUSH III. Alternatively spliced isoforms of the putative renal Na-K-Cl cotransporter are differentially distributed within the rabbit kidney. Proc. Natl. Acad. Sci. USA 91: 4544–4548, 1994.
Google Scholar
952 PAYNE, J. A., and B. FORBUSH III. Molecular characterization of the epithelial Na-K-Cl cotransporter isoforms. Curr. Opin. Cell Biol. 7: 493–503, 1995.
Google Scholar
953 PEAK M., AL-HABORI M., AGIUS L.Regulation of glycogen synthesis and glycolysis by insulin, pH and cell volume. Interactions between swelling and alkalinization in mediating the effects of insulin.Biochem. J.2821992797805
Crossref | PubMed | ISI | Google Scholar
954 PEARL M., TAYLOR A.Role of the cytoskeleton in the control of transcellular water flow by vasopressin in amphibian urinary bladder.Biol. Cell551985163172
Crossref | PubMed | ISI | Google Scholar
955 PECSVARADY Z., FISHER T. C., FABOK A., COATES T. D., MEISELMAN H. J.Kinetics of granulocyte deformability following exposure to chemotactic stimuli.Blood Cells181992333352
PubMed | Google Scholar
956 PEDERSEN S. F., KRAMHOFT B., JORGENSEN N. K., HOFFMANN E. K.Shrinkage-induced activation of the Na⁺/H⁺ exchanger in Ehrlich ascites tumor cells: mechanisms involved in the activation and a role for the exchanger in cell volume regulation.J. Membr. Biol.1491996141159
Crossref | PubMed | ISI | Google Scholar
957 PEÑA-RASGADO C., KIMLER V. A., McGRUDER K. D., TIE J., RASGADO-FLORES H.Opposite roles of cAMP and cGMP on volume loss in muscle cells.Am. J. Physiol.267(Cell Physiol. 36)1994C1319C1328
Link | Google Scholar
958 PEÑA-RASGADO C., McGRUDER K. D., SUMMERS J. C., RASGADO-FLORES H.Effect of isosmotic removal of extracellular Ca²⁺ and of membrane potential on cell volume in muscle cells.Am. J. Physiol.267(Cell Physiol. 36)1994C768C775
Link | Google Scholar
959 PEÑA-RASGADO C., SUMMERS J. C., McGRUDER K. D., DESANTIAGO J., RASGADO-FLORES H.Effect of isosmotic removal of extracellular Na⁺ on cell volume and membrane potential in muscle cells.Am. J. Physiol.267(Cell Physiol. 36)1994C759C767
Link | Google Scholar
960 PENDERGRASS W. R., ANGELLO J. C., KIRSCHNER M. D., NORWOOD T. H.The relationship between the rate of entry into S phase, concentration of DNA polymerase alpha, and cell volume in human diploid fibroblast-like monokaryon cells.Exp. Cell Res.1921991418425
Crossref | PubMed | ISI | Google Scholar
961 PENDERGRASS W. R., ANGELLO J. C., SAULEWICZ A. C., NORWOOD T. H.DNA polymerase alpha and the regulation of entry into S phase in heterokaryons.Exp. Cell Res.1921991426432
Crossref | PubMed | ISI | Google Scholar
962 PEREZ M., BARBER A., PONZ F.Effect of osmolarity on the epithelial paracellular permeabilty in rat jejunum.J. Physiol. Biochem.521996103112
ISI | Google Scholar
963 PERRY P. B., O'NEILL W. C.Swelling-activated K fluxes in vascular endothelial cells: volume regulation via K-Cl cotransport and K channels.Am. J. Physiol.265(Cell Physiol. 34)1993C763C769
Link | Google Scholar
964 PERSSON A. E., SALOMONSSON M., WESTERLUND P., GREGER R., SCHLATTER E., GONZALEZ E.Macula densa cell function.Kidney Int.32, Suppl.1991S39S44
Google Scholar
965 PESKIN C. S., ODELL G. M., OSTER G. F.Cellular motions and thermal fluctuations: the Brownian ratchet.Biophys. J.651993316324
Crossref | PubMed | ISI | Google Scholar
966 PETERSON D. P., MURPHY K. M., URSINO R., STREETER K., YANCEY P. H.Effects of dietary protein and salt on rat renal osmolytes: covariation in urea and GPC contents.Am. J. Physiol.263(Renal Fluid Electrolyte Physiol. 32)1992F594F600
Google Scholar
967 PETRONINI P. G., DE-ANGELIS E. M., BORGHETTI P., BORGHETTI A. F., WHEELER K. P.Modulation by betaine of cellular responses to osmotic stress.Biochem. J.28219926973
Crossref | PubMed | ISI | Google Scholar
968 PEWITT E. B., HEGDE R. S., HAAS M., PALFREY H. C.The regulation of Na/K/2Cl cotransport and bumetanide binding in avian erythrocytes by protein phosphorylation and dephosphorylation.J. Biol. Chem.26519902074720756
PubMed | ISI | Google Scholar
969 PFALLER W., WILLINGER C., STOLL B., HALLBRUCKER C., LANG F., HÄUSSINGER D.Structural reaction pattern of hepatocytes following exposure to hypotonicity.J. Cell. Physiol.1541993248253
Crossref | PubMed | ISI | Google Scholar
970 PIERCE S. K.Invertebrate cell volume control mechanisms: a coordinated use of intracellular amino acids and inorganic ions as osmotic solute.Biol. Bull.1631982405419
Crossref | ISI | Google Scholar
971 PIERCE S. K., POLITIS A. D.Ca²⁺-activated cell volume recovery mechanisms.Annu. Rev. Physiol.5219902742
Crossref | PubMed | ISI | Google Scholar
972 PINE M. B., BROOKS W. W., NOSTA J. J., ABELMANN W. H.Hydrostatic forces limit swelling of rat ventricular myocardium.Am. J. Physiol.241(Heart Circ. Physiol. 10)1981H740H747
Google Scholar
973 PINE M. B., RHODES D., THORP K., TSAI Y.Anion exchange and volume regulation during metabolic blockade of renal cortical slices.J. Physiol. (Lond.)2971979387403
Crossref | Google Scholar
974 PINTO L. H., HOLSINGER L. J., LAMB R. A.Influenza virus M2 protein has ion channel activity.Cell691992517528
Crossref | PubMed | ISI | Google Scholar
975 POLISCHUK T. M., ANDREW R. D.Real time imaging of intrinsic optical signals during early excitotoxicity evoked by domoic acid in the rat hippocampal slice.Can. J. Physiol. Pharmacol.741996712722
Crossref | PubMed | ISI | Google Scholar
976 PORONNIK P., SCHUMANN S. Y., COOK D. I.HCO⁻₃ dependent ACh-activated Na⁺ influx in sheep parotid secretory endpieces.Pflügers Arch.4291995852858
Crossref | PubMed | ISI | Google Scholar
977 POULIN R., WECHTER R. S., PEGG A. E.An early enlargement of the putrescine pool is required for growth in L1210 mouse leukemia cells under hyposmotic stress.J. Biol. Chem.266199161426151
PubMed | ISI | Google Scholar
978 PRAKASH V., LOUCHEUX C., SCHEUFELE S., GORBUNOFF M. J., TIMASHEFF S. N.Interactions of proteins with solvent components in 8 M urea.Arch. Biochem. Biophys.2101981455464
Crossref | PubMed | ISI | Google Scholar
979 PREDEL H. G., YANG Z., VON SEGESSER L., TURINA M., BÜHLER F. R., LÜSCHER T. F.Implications of pulsatile stretch on growth of saphenous vein and mammary artery smooth muscle.Lancet3401992878879
Crossref | PubMed | ISI | Google Scholar
980 PRESTON G. M., CARROLL T. P., GUGGINO W. P., AGRE P.Appearance of water channels in Xenopus oocytes expressing red cell CHIP28 protein.Science2561992385387
Crossref | PubMed | ISI | Google Scholar
981 PURO D. G., ROBERGE F., CHAN C. C.Retinal glial cell proliferation and ion channels: a possible link.Invest. Ophthalmol. Visual Sci.301989521529
PubMed | ISI | Google Scholar
982 RABKIN R., PALATHUMPAT M., TSAO T.Ammonium chloride alters renal tubular cell growth and protein turnover.Lab. Invest.681993427438
PubMed | ISI | Google Scholar
983 RADKE, K. J., R. E. CLENDENIN III, R. E. TAYLOR, Jr, and E. G. SCHNEIDER. Calcium dependence of osmolality-, potassium-, and angiotensin II-induced aldosterone secretion. Am. J. Physiol. 256 (Endocrinol. Metab. 19): E760–E764, 1989.
Google Scholar
984 RAJAGOPALAN K. V., FRIDOVICH I., HANDLER P.Competitive inhibition of enzyme activity by urea.J. Biol. Chem.236196110591065
PubMed | ISI | Google Scholar
985 RAND R. P., BURTON A. C.Mechanical properties of the red cell membrane. I. Membrane stiffness and intracellular pressure.Biophys. J.41964115135
Crossref | PubMed | ISI | Google Scholar
986 RAO G. N., DEROUX N., SARDET C., POUYSSEGUR J., BERK B.Na⁺/H⁺ antiporter gene expression precedes monocytic differentiation of HL60 cells (Abstract).FASEB J.51991A671
ISI | Google Scholar
987 RASGADO-FLORES H., PEÑA-RASGADO C., EHRENPREIS S.Cell volume and drug action: some interactions and perspectives.Drug Dev. Res.3619956180
Crossref | ISI | Google Scholar
988 RASOLA A., GALIETA L. J., GRUENERT D. C., ROMEO G.Volume-sensitive chloride currents in four epithelial cell lines are not directly correlated to the expression of the MDR-1 gene.J. Biol. Chem.269199414321436
PubMed | ISI | Google Scholar
989 RAYMOND J. A.Glycerol is a colligative antifreeze in some northern fishes.J. Exp. Zool.2621992347352
Crossref | Google Scholar
990 REDDY V. N., LIN L. R., GIBLIN F. J., CHAKRAPANI B., YOKOYAMA T.Study of the polyol pathway and cell permeability changes in human lens and retinal pigment epithelium in tissue culture.Invest. Ophthalmol. Visual Sci.33199223342339
PubMed | ISI | Google Scholar
991 REEVES W. B., GURICH R. W.Calcium-dependent chloride channels in endosomes from rabbit kidney cortex.Am. J. Physiol.266(Cell Physiol. 35)1994C741C750
Link | Google Scholar
992 REINACH P. S., TARVIN J. T., HIRSCH M.Changes in cellular membrane and paracellular conductances by amphotericin B in the epithelium of the bullfrog cornea.Biochim. Biophys. Acta10661991115123
Crossref | PubMed | ISI | Google Scholar
993 REUNER K. H., SCHLEGEL K., JUST I., AKTORIES K., KATZ N.Autoregulatory control of actin synthesis in cultured rat hepatocytes.FEBS Lett.2861991100104
Crossref | PubMed | ISI | Google Scholar
994 REUSS L., ALTENBERG G. A.cAMP-activated Cl⁻ channels: regulatory role in gallbladder and other absorptive epithelia.News Physiol. Sci.1019958691
Abstract | Google Scholar
995 REUSS, L., and C. U. COTTON. Volume regulation in epithelia: transcellular transport and cross-talk. In: Cellular and Molecular Physiology of Cell Volume Regulation, edited by K. Strange. Boca Raton, FL: CRC, 1994, p. 31–47.
Google Scholar
996 REY O., ROSSI J. P. F. C., LOPEZ R., IAPALUCCI-ESPINOZA S. J., FRANZE-FERNANDEZ M. T.Tacaribe virus infection may induce inhibition of the activity of the host cell Ca²⁺ and Na⁺/K⁺ pumps.J. Gen. Virol.691988951954
Crossref | PubMed | ISI | Google Scholar
997 RICHTER E. A., CLELAND P. J., RATTIGAN S., CLARK M. G.Contraction-associated translocation of protein kinase C in rat sceletal muscle.FEBS Lett.2171987232236
Crossref | PubMed | ISI | Google Scholar
998 RICK R.Ion concentration changes in renal cells during regulatory volume decrease.Am. J. Physiol.265(Renal Fluid Electrolyte Physiol. 34)1993F77F86
Google Scholar
999 RIEPE M., CARPENTER D. O.Delayed increase of cell volume of single pyramidal cells in live rat hippocampal slices upon kainate application.Neurosci. Lett.19119953538
Crossref | PubMed | ISI | Google Scholar
1000 RITTER M., WÖLL E.Modification of cellular ion transport by the Ha-ras oncogene: steps towards malignant transformation.Cell. Physiol. Biochem.61996245270
Crossref | ISI | Google Scholar
1001 RITTER M., DARTSCH P., WALDEGGER S., HALLER T., ZWIERZINA H., LANG H. J., LANG F.Effects of bradykinin on NIH 3T3 fibroblasts pretreated with lithium-mimicking events of Ha-ras oncogene expression.Biochim. Biophys. Acta135819972030
ISI | Google Scholar
1002 RITTER M., PAULMICHL M., LANG F.Further characterization of volume regulatory decrease in cultured renal epitheloid (MDCK) cells.Pflügers Arch.41819913539
Crossref | PubMed | ISI | Google Scholar
1003 RITTER M., SCHRATZBERGER P., WÖLL E.CH. KÄHLER, N. REINISCH, F. LANG, and C. H. WIEDERMANN. Cell volume regulatory ion transport mechanisms involved in the regulation of neutrophil leucocyte migration (Abstract).Pflügers Arch.431S1996P227
Google Scholar
1004 RITTER M., WÖLL E., HALLER T., DARTSCH P. C., ZWIERZINA H., LANG F.Activation of the Na⁺/H⁺ exchanger by the transforming Ha-ras requires stimulated cellular calcium influx and is associated with rearrangement of the actin cytoskeleton.Eur. J. Cell Biol.721997222228
PubMed | ISI | Google Scholar
1005 RITTER M., WÖLL E., HÄUSSINGER D., LANG F.Effects of bradykinin on cell volume and intracellular pH in NIH 3T3 fibroblasts expressing the ras oncogene.FEBS Lett.3071992367370
Crossref | PubMed | ISI | Google Scholar
1006 RITTER M., WÖLL E., WALDEGGER S., HÄUSSINGER D., LANG H. J., SCHOLZ W., SCHÖLKENS B., LANG F.Cell shrinkage stimulates bradykinin induced cell membrane potential oscillations in NIH 3T3 fibroblasts expressing the ras-oncogene.Pflügers Arch.4231993221224
Crossref | PubMed | ISI | Google Scholar
1007 RIVAS T., URCELAY E., MANCHON-GONZALEZ C., PARILLA R., AYUSO M. S.Role of amino acid-induced changes in ion fluxes in the regulation of hepatic protein synthesis.J. Cell. Physiol.1631995277284
Crossref | PubMed | ISI | Google Scholar
1008 ROBBINS E., PEDERSON T., KLEIN P.Comparison of mitotic phenomena and effects induced by hyperonic solutions in HeLa cells.J. Cell Biol.441970400416
Crossref | PubMed | ISI | Google Scholar
1009 ROBERTSON M. A., FOSKETT J. K.Na⁺ transport pathways in secretory acinar cells: membrane cross talk mediated by [Cl⁻]_i .Am. J. Physiol.267(Cell Physiol. 36)1994C146C156
Link | Google Scholar
1010 ROBINSON, A. G., and J. N. LOEB. Ethanol ingestion: commonest cause of elevated plasma osmolality? N. Engl. J. Med. 284: 1253–1255, 1971.
Google Scholar
1011 ROBINSON C. R., SLIGAR S. G.Molecular recognition mediated by bound water. A mechanism for star activity of the restriction endonuclease EcoRI.J. Mol. Biol.2341993302306
Crossref | PubMed | ISI | Google Scholar
1012 ROBSON L., HUNTER M.Volume regulatory responses in frog isolated proximal cells.Pflügers Arch.42819946068
Crossref | PubMed | ISI | Google Scholar
1013 ROBSON L., HUNTER M.Role of cell volume and protein kinase C in regulation of a Cl⁻ conductance in single proximal tubule cells of Rana temporaria.J. Physiol. (Lond.)480199417
Crossref | Google Scholar
1014 ROBSON L., HUNTER M.Regulation of an outwardly rectifying Cl conductance in single proximal tubule cells isolated from frog kidney.J. Physiol. (Lond.)4981997409417
Crossref | Google Scholar
1015 ROEPE P. D., WEISBURG J. H., LUZ J. G., HOFFMAN M. M., WEI L.-Y.Novel Cl⁻ dependent intracellular pH regulation in murine MDR 1 transfectants and potential implications.Biochemistry3319941100811015
Crossref | PubMed | ISI | Google Scholar
1016 ROME L., LECHENE C., SAVIN V., GRANTHAM J.Critical role of short-chain fatty acids in isovolumetric regulation (IVR) of proximal S2 segments in hyperosmotic media (Abstract).Kidney Int.331988438
ISI | Google Scholar
1017 ROSALES O. R., SUMPIO B. E.Changes in cyclic strain increase inositol triphosphate and diacylglycerol in endothelial cells.Am. J. Physiol.262(Cell Physiol. 31)1992C956C962
Link | Google Scholar
1018 ROSEN S. D., BERTOZZI C. R.The selectins and their ligands.Curr. Opin. Cell Biol.61994663673
Crossref | PubMed | ISI | Google Scholar
1019 ROSENGREN S., HENSON P. M., WORTHEN G. S.Migration-associated volume changes in neutrophils facilitate the migratory process in vitro.Am. J. Physiol.267(Cell Physiol. 36)1994C1623C1632
Link | Google Scholar
1020 ROSETTE C., KARIN M.Ultraviolet light and osmotic stress: activation of the JNK cascade through multiple growth factor and cytokine receptors.Science274199611941197
Crossref | PubMed | ISI | Google Scholar
1021 ROSS B. D., JACOBSON S., VILLAMIL F., KORULA J., KREIS R., ERNST T., SHONK T., MOATS R. A.Subclinical hepatic encephalopathy: proton MR spectroscopic abnormalities.Radiology1931994457463
Crossref | PubMed | ISI | Google Scholar
1022 ROSSKOPF D., DÜSING R., SIFFERT W.Membrane sodium-proton exchange and primary hypertension.Hypertension211993607617
Crossref | PubMed | ISI | Google Scholar
1023 ROSSKOPF D., FRÖMTER E., SIFFERT W.Hypertensive sodium-proton exchanger phenotype persists in immortalized lymphoblasts from essential hypertensive patients. A cell culture model for human hypertension.J. Clin. Invest.92199325532559
Crossref | PubMed | ISI | Google Scholar
1024 ROSSKOPF D., HAIDER N., QUEDNAU B., SIFFERT W.Expression and activity of the Na⁺/H⁺ exchanger NHE-1 in various tissues of spontaneously hypertensive rats and normotensive Wistar-Kyoto rats.Cell. Physiol. Biochem.51995276285
Crossref | ISI | Google Scholar
1025 ROSSKOPF D., SCHOLZ W., LANG H. J., SCHÖLKENS B. A., SIFFERT W.HOE 694 blocks Na⁺/H⁺ exchange in human B lymphoblasts without influencing proliferation.Cell Physiol. Biochem.51995269275
Crossref | ISI | Google Scholar
1026 ROSSKOPF D., SCHRÖDER K.-J., SIFFERT W.Role of sodium-hydrogen exchange in the proliferation of immortalised lymphoblasts from patients with essential hypertension and normotensive subjects.Cardiovasc. Res.291995254259
Crossref | PubMed | ISI | Google Scholar
1027 ROTH E., ZÖCH G., SCHULZ F., KARNER J., MÜHLBACHER F., HAMILTON G., MAURITZ W., SPORN P., FUNOVICS J.Amino acid concentrations in plasma and skeletal muscle of patients with acute hemorrhagic necrotizing pancreatitis.Clin. Chem.31198513051309
PubMed | ISI | Google Scholar
1028 ROTHSTEIN A., MACK E.Actions of mercurials on cell volume regulation of dissociated MDCK cells.Am. J. Physiol.260(Cell Physiol. 29)1991C113C121
Link | Google Scholar
1029 ROTHSTEIN A., MACK E.Volume-activated K⁺ and Cl⁻ pathways of dissociated epithelial cells (MDCK): role of Ca²⁺.Am. J. Physiol.258(Cell Physiol. 27)1990C827C834
Link | Google Scholar
1030 ROTOLI B. M., BUSSOLATI O., DALLASTA V., HOFFMANN E. K., CABRINI G., GAZZOLA G. C.CFTR expression in C127 cells is associated with enhanced cell shrinkage and ATP extrusion in Cl-free medium.Biochem. Biophys. Res. Commun.2271996755761
Crossref | PubMed | ISI | Google Scholar
1031 ROUGIER J. P., MOULLIER P., PIEDAGNEL R., RONCO P. M.Hyperosmolality suppresses but TGF beta 1 increases MMP9 in human peritoneal mesothelial cells.Kidney Int.511997337347
Crossref | PubMed | ISI | Google Scholar
1032 ROWE W. A., BLACKMON D. L., MONTROSE M. H.Propionate activates multiple ion transport mechanisms in the HT29–18-Cl human colon cell line.Am. J. Physiol.265(Gastrointest. Liver Physiol. 28)1993G564G571
Google Scholar
1033 ROY, D. R., H. E. LAYTON, and R. L. JAMISON. Countercurrent mechanism and its regulation. In: The Kidney: Physiology and Pathophysiology (2nd ed.), edited by D. W. Seldin and G. Giebisch. New York: Raven, 1992, p. 1649–1692.
Google Scholar
1034 ROY G., BANDERALI U.Channels for ions and amino acids in kidney cultured cells (MDCK) during volume regulation.J. Exp. Zool.2681994121126
Crossref | PubMed | Google Scholar
1035 RUDEL T., SCHMIDT A., BENZ R., KOLB H. A., LANG F., MEYER T. F.Modulation of Neisseria porin (PorB) by cytosolic ATP/GTP of target cells: parallels between pathogen accommodation and mitochondrial endosymbiosis.Cell851996391402
Crossref | PubMed | ISI | Google Scholar
1036 RUEPP B., BOHREN K. M., GABBAY K. H.Characterization of the osmotic response element of the human aldose reductase gene promoter.Proc. Natl. Acad. Sci. USA93199686248629
Crossref | PubMed | ISI | Google Scholar
1037 RUHFUS B., TINEL H., KINNE R. K. H.Role of G proteins in the regulation of organic osmolyte efflux from isolated rat renal inner medullary collecting duct cells.Pflügers Arch.43319963541
Crossref | PubMed | ISI | Google Scholar
1038 RUSSO M. A., ERNST S. A., KAPOOR S. C., VAN ROSSUM G. D. V.Morphological and physiological studies of rat kidney cortex slices undergoing isosmotic swelling and its reversal: a possible mechanism for ouabain-resistant control of cell volume.J. Membr. Biol.851985124
Crossref | PubMed | ISI | Google Scholar
1039 RUSSO M. A., MORGANTE E., MARIANI M. F., YEH H. I., FARBER J. L., VAN ROSSUM G. D.Effects of ouabain and chloride-free medium on isosmotic volume control and ultrastructure of hepatocytes in primary culture.Eur. J. Cell Biol.641994229242
PubMed | ISI | Google Scholar
1040 SACHS F.Mechanical transduction by membrane ion channels: a mini review.Mol. Cell. Biochem.10419915760
Crossref | PubMed | ISI | Google Scholar
1041 SACHS J. R., MARTIN D. W.The role of ATP in swelling-stimulated K-Cl cotransport in human red cell ghosts. Phosphorylation-dephosphorylation events are not in the signal transduction pathway.J. Gen. Physiol.1021993551573
Crossref | PubMed | ISI | Google Scholar
1042 SACKIN H.Stretch-activated potassium channels in renal proximal tubule.Am. J. Physiol.253(Renal Fluid Electrolyte Physiol. 22)1987F1253F1262
Google Scholar
1043 SACKIN, H. Stretch-activated ion channels. In: Cellular and Molecular Physiology of Cell Volume Regulation, edited by K. Strange. Boca Raton, FL: CRC, 1994, p. 215–240.
Google Scholar
1044 SADOSHIMA J., QUI Z. H., MORGAN J. P., IZUMO S.Tyrosine kinase activation is an immediate and essential step in hypotonic cell swelling induced ERK activation and c-Fos gene expression in cardiac myocytes.EMBO J.15199655355546
Crossref | PubMed | ISI | Google Scholar
1045 SAHA N., SCHREIBER R., VOM S.DAHL, F. LANG, W. GEROK, and D. HÄUSSINGER. Endogenous hydroperoxide formation, cell volume and cellular K⁺ balance in perfused rat liver.Biochem. J.2961993701707
Crossref | PubMed | ISI | Google Scholar
1046 SAHA N., STOLL B., LANG F., HÄUSSINGER D.Effect of anisotonic cell volume modulation on glutathione-S-conjugate release, t-butylhydroperoxide metabolism and the pentose-phosphate shunt in perfused rat liver.Eur. J. Biochem.2091992437444
Crossref | PubMed | Google Scholar
1047 SAKAI H., KAKINOKI B., DIENER M., TAKEGUCHI N.Endogenous arachidonic acid inhibits hypotonically activated Cl channels in isolated rat hepatocytes.Jpn. J. Physiol.461996311318
Crossref | PubMed | Google Scholar
1048 SALTIN, B., G. SJØGAARD, S. STRANGE, and C. JUEL. Redistribution of K⁺ in the human body during muscular exercise: its role to maintain whole body homeostasis. In: Man in Stressful Environments: Thermal and Work Physiology, edited by K. Shiraki and M. K. Yousef. Springfield, IL: Thomas, 1987, p. 247–267.
Google Scholar
1049 SANCHEZ-OLEA R., FULLER C., BENOS D., PASANTES-MORALES H.Volume-associated osmolyte fluxes in cell lines with or without the anion exchanger.Am. J. Physiol.269(Cell Physiol. 38)1995C1280C1286
Link | Google Scholar
1050 SANCHEZ-OLEA R., MORAN J., SCHOUSBOE A., PASANTES-MORALES H.Hyposmolarity-activated fluxes of taurine in astrocytes are mediated by diffusion.Neurosci. Lett.1301991233236
Crossref | PubMed | ISI | Google Scholar
1051 SANCHEZ-OLEA R., MORALES-MULIA M., MORAN J., PASANTES-MORALES H.Inhibition by dihydropyridines of regulatory volume decrease and osmolyte fluxes in cultured astrocytes is unrelated to extracellular calcium.Neurosci. Lett.1931995165168
Crossref | PubMed | ISI | Google Scholar
1052 SANCHEZ-OLEA R., MORALES-MULIA M., MORAN J., PASANTES-MORALES H.Inhibition of polyunsaturated fatty acids of cell volume regulation and osmolyte fluxes in astrocytes.Am. J. Physiol.269(Cell Physiol. 38)1995C96C102
Link | Google Scholar
1053 SANDS, J. M. Regulation of intracellular polyols and sugars in response to osmotic stress. In: Cellular and Molecular Physiology of Cell Volume Regulation, edited by K. Strange. Boca Raton, FL: CRC, 1994, p. 133–146.
Google Scholar
1054 SANDS J. M., SCHRADER D. C.Coordinated response of renal medullary enzymes regulating net sorbitol production in diuresis and antidiuresis.J. Am. Soc. Nephrol.119905865
PubMed | ISI | Google Scholar
1055 SANDS J. M., TERADA Y., BERNARD L. M., KNEPPER M. A.Aldose reductase activities in microdissected rat renal tubule segments.Am. J. Physiol.256(Renal Fluid Electrolyte Physiol. 25)1989F563F569
Google Scholar
1056 SANDVIG K., OLSNES S., PETERSEN O. W., VAN DEURS B.Acidification of the cytosol inhibits endocytosis from coated pits.J. Cell Biol.1051987679689
Crossref | PubMed | ISI | Google Scholar
1057 SANTELL L., RUBIN R. L., LEVIN E. G.Enhanced phosphorylation and dephosphorylation of a histone-like protein in response to hyperosmotic and hyposmotic conditions.J. Biol. Chem.26819932144321447
PubMed | ISI | Google Scholar
1058 SANTORO M. M., LIU Y., KHAN S. M. A., HOU L.-X., BOLEN D. W.Increased thermal stability of proteins in the presence of naturally occurring osmolytes.Biochemistry31199252785283
Crossref | PubMed | ISI | Google Scholar
1059 SARANSAARI P., OJA S. S.Excitatory amino acids evoke taurine release from cerebral cortex slices from adult and developing mice.Neuroscience451991451459
Crossref | PubMed | ISI | Google Scholar
1060 SARKADI B., MACK E., ROTHSTEIN A.Ionic events during the volume response of human peripheral blood lymphocytes to hypotonic media. I. Distinctions between volume-activated Cl⁻ and K⁺ conductance pathways.J. Gen. Physiol.831984497512
Crossref | PubMed | ISI | Google Scholar
1061 SARKADI B., PARKER J. C.Activation of ion transport pathways by changes in cell volume.Biochim. Biophys. Acta10711991407427
Crossref | PubMed | ISI | Google Scholar
1062 SATO N., MURAKAMI M., WANG X., GREER M. A.The contrasting role of calcium influx in secretion induced by cell swelling can differentiate normal and tumor-derived rat pituitary cells.Endocrinology129199125412546
Crossref | PubMed | ISI | Google Scholar
1063 SATO N., WANG X., GREER M. A.Hormone secretion stimulated by ethanol-induced cell swelling in normal rat adenohypophysial cells.Am. J. Physiol.260(Endocrinol. Metab. 23)1991E946E950
Google Scholar
1064 SATO N., WANG X., GREER M. A.Dopamine inhibits cell swelling-induced prolactin secretion in MMQ cells by blocking Ca²⁺ influx.Mol. Cell. Endocrinol.82199199106
Crossref | PubMed | ISI | Google Scholar
1065 SATO N., WANG X., GREER M. A.Medium hyperosmolarity depresses thyrotropin-releasing hormone-induced Ca²⁺ influx and prolactin secretion in GH₄C₁ cells.Mol. Cell. Endocrinol.771991193198
Crossref | PubMed | ISI | Google Scholar
1066 SATO N., WANG X., GREER M. A.Protein kinase C modulates cell swelling-induced Ca²⁺ influx and prolactin secretion in GH₄C₁ cells.Mol. Cell. Endocrinol.861992137142
Crossref | PubMed | ISI | Google Scholar
1067 SATO N., WANG X., GREER M. A.The rate of increase not the amplitude of cytosolic Ca²⁺ regulates the degree of prolactin secretion induced by depolarizing K⁺ or hyposmolarity in GH₄C₁ cells.Biochem. Biophys. Res. Commun.1701990968972
Crossref | PubMed | ISI | Google Scholar
1068 SATO N., WANG X., GREER M. A., GREER S. E., McADAMS S.Evidence that ethanol induces prolactin secretion in GH₄C₁ cells by producing cell swelling with resultant calcium influx.Endocrinology127199030793086
Crossref | PubMed | ISI | Google Scholar
1069 SATO N., WANG X., GREER M. A., GREER S. E., McADAMS S.The permeant molecule urea stimulates prolactin secretion in GH₄C₁ cells by inducing Ca²⁺ influx through dihydropyridine-sensitive Ca²⁺ channels.Mol. Cell. Endocrinol.701990273279
Crossref | PubMed | ISI | Google Scholar
1070 SATO N., WANG X., GREER M. A., GREER S. E., McADAMS S., OSHIMA T.Medium hyposmolarity stimulates prolactin secretion in GH₄C₁ cells by inducing an increase in cytosolic free calcium.Endocrinology1271990957964
Crossref | PubMed | ISI | Google Scholar
1071 SCHIEBINGER R. J., LINDEN J.The influence of resting tension on immunoreactive atrial natriuretic peptide secretion by rat atria superfused in vitro.Circ. Res.591986105109
Crossref | PubMed | ISI | Google Scholar
1072 SCHLIESS F., SCHREIBER R., HÄUSSINGER D.Activation of extracellular signal-regulated kinases Erk-1 and Erk-2 by cell swelling in H4IIE hepatoma cells.Biochem. J.30919951317
Crossref | PubMed | ISI | Google Scholar
1073 SCHLIESS F., SINNING R., FISCHER R., SCHMALENBACH C., HÄUSSINGER D.Calcium dependent activation of ERK 1 and ERK 2 after hypoosmotic astrocyte swelling.Biochem. J.3201996167171
Crossref | PubMed | ISI | Google Scholar
1074 SCHLOTTMANN K., COGGESHALL K. M.CD95/Fas/Apo-1-mediated signal transduction.Cell. Physiol. Biochem.61996345360
Crossref | ISI | Google Scholar
1075 SCHMOLKE M., BECK F. X., GUDER W. G.Effect of antidiuretic hormone on renal organic osmolytes in Brattleboro rats.Am. J. Physiol.257(Renal Fluid Electrolyte Physiol. 26)1989F732F737
Google Scholar
1076 SCHMOLKE M., BORNEMANN A., GUDER W. G.Polyol determination along the rat nephron.Biol. Chem. Hoppe-Seyler3711990909916
Crossref | PubMed | ISI | Google Scholar
1077 SCHMOLKE, M., A. BORNEMANN, and W. G. GUDER. Distribution and regulation of organic osmolytes along the nephron. In: Cellular and Molecular Biology of the Kidney, edited by H. Koide, H. Endou, and K. Kurokawa. Basel: Karger, 1991, p. 255–263.
Google Scholar
1078 SCHMOLKE M., GUDER W. G.Metabolic regulation of organic osmolytes in tubules from rat renal inner and outer medulla.Renal Physiol. Biochem.121989347358
PubMed | Google Scholar
1079 SCHMOLKE M., SCHLEICHER E., GUDER W. G.Renal sorbitol, myo-inositol and glycerophosphorylcholine in streptozotocin-diabetic rats.Eur. J. Clin. Chem. Clin. Biochem.301992607614
PubMed | Google Scholar
1080 SCHNEIDER E. G.In water deprivation, osmolality becomes an important determinant of aldosterone secretion.News Physiol. Sci.51990197201
Abstract | Google Scholar
1081 SCHNEIDER E. G., KRAMER R. E.Effect of osmolality on angiotensin-stimulated aldosterone production by primary cultures of bovine adrenal glomerulosa cells.Biochem. Biophys. Res. Commun.13919864651
Crossref | PubMed | ISI | Google Scholar
1082 SCHNEIDER E. G., RADKE K. J., ULDERICH D., TAYLOR R. E.Jr. Effect of osmolality on aldosterone secretion.Endocrinology116198516211626
Crossref | PubMed | ISI | Google Scholar
1083 SCHNEIDER E. G., TAYLOR R. E.Jr., K. J. RADKE, and P. G. DAVIS. Effect of sodium concentration on aldosterone secretion by isolated perfused canine adrenal glands.Endocrinology115198421952204
Crossref | PubMed | ISI | Google Scholar
1084 SCHNEIDER G.-H., BAETHMANN A., KEMPSKI O.Mechanisms of glial swelling induced by glutamate.Can. J. Physiol. Pharmacol.70, Suppl.1992S334S343
Crossref | PubMed | ISI | Google Scholar
1085 SCHOLZ W., ALBUS U., LANG H. J., LINZ W., MARTORANA P. A., ENGLERT H. C., SCHÖLKENS B. A.HOE 694, a new Na⁺/H⁺ exchange inhibitor and its effects in cardiac ischaemia.Br. J. Pharmacol.1091993562568
Crossref | PubMed | ISI | Google Scholar
1086 SCHOUSBOE A., PASANTES-MORALES H.Role of taurine in neural cell volume regulation.Can. J. Physiol. Pharmacol.70, Suppl.1992S356S361
Crossref | PubMed | ISI | Google Scholar
1087 SCHOUSBOE A., SANCHEZ-OLEA R., MORAN J., PASANTES-MORALES H.Hyposmolarity-induced taurine release in cerebellar granule cells is associated with diffusion and not with high-affinity transport.J. Neurosci. Res.301991661665
Crossref | PubMed | ISI | Google Scholar
1088 SCHREIBER R., HÄUSSINGER D.Characterization of the swelling-induced alkalinization of endocytotic vesicles in fluorescein isothiocyanate-dextran-loaded rat hepatocytes.Biochem. J.30919951924
Crossref | PubMed | ISI | Google Scholar
1089 SCHREIBER R., STOLL B., LANG F., HÄUSSINGER D.Effects of aniso-osmolarity and hydroperoxides on intracellular pH in isolated rat hepatocytes as assessed by (2′,7′)-bis(carboxyethyl)-5(6)-carboxyfluorescein and fluorescein isothiocyanate-dextran fluorescence.Biochem. J.3031994113120
Crossref | PubMed | ISI | Google Scholar
1090 SCHREIBER R., ZHANG F., HÄUSSINGER D.Regulation of vesicular pH in liver macrophages and parenchymal cells by ammonia and anisotonicity as assessed by fluorescein isothiocyanate-dextran fluorescence.Biochem. J.3151996385392
Crossref | PubMed | ISI | Google Scholar
1091 SCHULLER H. M., ORLOFF M., REZNIK G. K.Antiproliferative effects of the Ca²⁺/calmodulin antagonist B859–35 and the Ca²⁺-channel blocker verapamil on human lung cancer cell lines.Carcinogenesis12199123012303
Crossref | PubMed | ISI | Google Scholar
1092 SCHULTZ, S. G. Homocellular regulatory mechanisms in sodium-transporting epithelia: avoidance of extinction by “flush-through.” Am. J. Physiol. 241 (Renal Fluid Electrolyte Physiol. 10): F579–F590, 1981.
Google Scholar
1093 SCHULTZ, S. G. Membrane cross-talk in sodium-absorbing epithelial cells. In: The Kidney: Physiology and Pathophysiology (2nd ed.), edited by D. W. Seldin and G. Giebisch. New York: Raven, 1992, vol. 11, p. 287.
Google Scholar
1094 SCHULTZ S. G.The “Pump-Leak” parallelism in Necturus enterocytes: some cellular and molecular insights.Renal Physiol. Biochem.171994134137
PubMed | Google Scholar
1095 SCHULTZ S. G.Volume preservation: then and now.News Physiol. Sci.41989169172
Abstract | Google Scholar
1096 SCHULTZ S. G., HUDSON R. L., LAPOINTE J.-Y.Electrophysiological studies of sodium cotransport in epithelia: towards a cellular model.Ann. NY Acad. Sci.4561985127135
Crossref | PubMed | ISI | Google Scholar
1097 SCHULTZ W. A., EICKELMANN P., HALLBRUCKER C., SIES H., HÄUSSINGER D.Increase of β-actin mRNA upon hypotonic perfusion of perfused rat liver.FEBS Lett.2921991264266
Crossref | PubMed | ISI | Google Scholar
1098 SCHWAB A., FINSTERWALDER F., KERSTING U., DANKER T., OBERLEITHNER H.Intracellular Ca²⁺ distribution in migrating transformed renal epithelial cells.Pflügers Arch.43419977076
Crossref | PubMed | ISI | Google Scholar
1099 SCHWAB A., GABRIEL K., FINSTERWALDER F., FOLPRECHT G., GREGER R., KRAMER A., OBERLEITHNER H.Polarized ion transport during migration of transformed Madin-Darby canine kidney cells.Pflügers Arch.4301995802807
Crossref | PubMed | ISI | Google Scholar
1100 SCHWAB A., OBERLEITHNER H.Plasticity of renal epithelial cells: the way a potassium channel supports migration.Pflügers Arch.432Suppl.1996R87R93
Google Scholar
1101 SCHWAB A., WOJNOWSKI L., GABRIEL K., OBERLEITHNER H.Oscillating activity of a Ca²⁺-sensitive K⁺ channel. A prerequisite for migration of transformed Madin-Darby canine kidney focus cell.J. Clin. Invest.93199416311636
Crossref | PubMed | ISI | Google Scholar
1102 SCHWARTZ G. J., ZAVILOWITZ B. J., RADICE A. D., GARCIA-PÉREZ A., SANDS J. M.Maturation of aldose reductase expression in the neonatal rat inner medulla.J. Clin. Invest.90199212751283
Crossref | PubMed | ISI | Google Scholar
1103 SCHWARTZ M. A., BOTH G., LECHENE C.The effect of cell spreading on cytoplasmic pH in normal and transformed fibroblasts.Proc. Natl. Acad. Sci. USA86198945254529
Crossref | PubMed | ISI | Google Scholar
1104 SCHWARTZ M. A., CRAGOE E. J.Jr., and C. LECHENE. pH regulation in spread cells and round cells.J. Biol. Chem.265199013271332
PubMed | ISI | Google Scholar
1105 SCHWARTZ M. A., LECHENE C.Adhesion is required for protein kinase C-dependent activation of the Na⁺/H⁺ antiporter by platelet-derived growth factor.Proc. Natl. Acad. Sci. USA89199261386141
Crossref | PubMed | ISI | Google Scholar
1106 SCHWARTZ M. A., LECHENE C., INGBER D. E.Insoluble fibronectin activates the Na/H antiporter by clustering and immobilizing integrin α5β1, independent of cell shape.Proc. Natl. Acad. Sci. USA88199178497853
Crossref | PubMed | ISI | Google Scholar
1107 SCHWIEBERT E. M., KARLSON K. H., FRIEDMAN P. A., DIETL P., SPIELMAN W. S., STANTON B. A.Adenosine regulates a chloride channel via protein kinase C and a G protein in a rabbit cortical collecting duct cell line.J. Clin. Invest.891992834841
Crossref | PubMed | ISI | Google Scholar
1108 SCHWIEBERT E. M., MILLS J. W., STANTON B. A.Actin-based cytoskeleton regulates a chloride channel and cell volume in a renal cortical collecting duct cell line.J. Biol. Chem.269199470817089
PubMed | ISI | Google Scholar
1109 SEMPLICINI A., MARZOLA M., MOZZATO G., CEOLOTTO G., PESSINA A. C.Red blood cell Li⁺/Na⁺ exchange in patients with diabetic nephropathy and essential hypertension: therapeutic implications.Renal Failure151993331338
Crossref | PubMed | ISI | Google Scholar
1110 SEN C. K., HANNINEN O., ORLOV S. N.Unidirectional sodium and potassium flux in myogenic L6 cells: mechanisms and volume dependent regulation.J. Appl. Physiol.781995272281
Link | ISI | Google Scholar
1111 SEO J. T., LARCOMBE-McDOUALL J. B., CASE R. M., STEWARD M. C.Modulation of Na⁺-H⁺ exchange by altered cell volume in perfused rat mandibular salivary gland.J. Physiol. (Lond.)4871995185195
Crossref | Google Scholar
1112 SERGEEV I. I. U., TARASOVA O. S., MEDVEDEVA N. A.An analysis of the components of the hyperosmotic vasomotor effect.Fiziol. Zh.3819923642
PubMed | ISI | Google Scholar
1113 SERNKA T. J.Direct hyposmotic stimulation of gastric acid secretion.Membr. Biochem.9199017
Crossref | PubMed | ISI | Google Scholar
1114 SETTMACHER U., VOLK H. D., VON BAEHR R., WOLFF H., JAHN S.In vitro stimulation of human fetal lymphocytes by mitogens and interleukins.Immunol. Lett.351993147152
Crossref | PubMed | ISI | Google Scholar
1115 SHEIK-HAMAD D., FERRARIS J. D., DRAGOLOVICH J., PREUSS H. G., BURG M. B.and A. GARCIA-PEREZ. CD9 antigen mRNA is induced by hypertonicity in two renal epithelial cells lines.Am. J. Physiol.270(Cell Physiol. 39)1996C253C258
Link | Google Scholar
1116 SHEIK-HAMAD D., GARCIA-PEREZ A., FERRARIS J. D., PETERS E. M., BURG M. B.Induction of gene expression by heat shock versus osmotic stress.Am. J. Physiol.267(Renal Fluid Electrolyte Physiol. 36)1994F28F34
Google Scholar
1117 SHEIKOV N.Immune activation of guinea pig lymphocytes type “cerebriform” and type “hand mirror.” An ultrastructural study.Cell Mol. Biol.391993829833
PubMed | ISI | Google Scholar
1118 SHEPPARD D. N., RICH D. P., OSTEDGAARD L. S., GREGORY R. J., SMITH A. E., WELSH M. J.Mutations in CFTR associated with mild-disease-form Cl⁻ channels with altered pore properties.Nature3621993160164
Crossref | PubMed | ISI | Google Scholar
1119 SHIFRIN S., PARROTT C. L.Influence of glycerol and other polyhydric alcohols on the quaternary structure of an oligomeric protein.Arch. Biochem. Biophys.1661975426432
Crossref | PubMed | ISI | Google Scholar
1120 SHIGA N., WANGEMANN P.Ion selectivity of volume regulatory mechanisms present during a hyposmotic challenge in vestibular dark cells.Biochim. Biophys. Acta124019954854
Crossref | PubMed | ISI | Google Scholar
1121 SHIRVAN, M. H., and S. ROTTEM. Ion pumps and volume regulation in mycoplasma. In: Subcellular Biochemistry: Mycoplasma Cell Membranes, edited by S. Rottem and I. Kahane. New York: Plenum, 1993, p. 261–292.
Google Scholar
1122 SHONK T. K., MOATS R. A., GIFFORD P., MICHAELIS T., MANDIGO J. C., IZUMI J., ROSS B. D.Probable Alzheimer disease: diagnosis with proton MR spectroscopy.Radiology19519956572
Crossref | PubMed | ISI | Google Scholar
1123 SHULTZ P. J., RAIJ L.Inhibition of human mesangial cell proliferation by calcium channel blockers.Hypertension151990176180
Crossref | ISI | Google Scholar
1124 SIFFERT W., DÜSING R.Sodium-proton exchange and primary hypertension. An update.Hypertension26199517
Crossref | ISI | Google Scholar
1125 SILVER S. M., STERNS R. H., HALPERIN M. L.Brain swelling after dialysis: old urea or new osmoles.Am. J. Kidney Dis.281996113
Crossref | PubMed | ISI | Google Scholar
1126 SIMONSEN L. O., BROWN A. M., CHRISTENSEN S., HARBAK H., SVANE P. C., HOFFMANN E. K.Thrombin and bradykinin mimic the volume response induced by cell swelling in Ehrlich mouse ascites tumor cells.Renal Physiol. Biochem.131990176
Google Scholar
1127 SINNING R., SCHLIESS F., KUBITZ R., HÄUSSINGER D.Osmosignalling in C6 glioma cells.FEBS Lett.4001997163167
Crossref | PubMed | ISI | Google Scholar
1128 SKØTT O.Calcium and osmotic stimulation in renin release from isolated rat glomeruli.Pflügers Arch.4061986485491
Crossref | PubMed | ISI | Google Scholar
1129 SKØTT, O. Do osmotic forces play a role in renin secretion? Am. J. Physiol. 255 (Renal Fluid Electrolyte Physiol. 24): F1–F10, 1988.
Google Scholar
1130 SMARDO F. L., BURG M. B., GARCIA-PÉREZ A.Kidney aldose reductase gene transcription is osmotically regulated.Am. J. Physiol.262(Cell Physiol. 31)1992C776C782
Link | Google Scholar
1131 SMITH T. W., RASMUSSON R. L., LOBAUGH L. A., LIEBERMAN M.Na⁺/K⁺ pump inhibition induces cell shrinkage in cultured chick cardiac myocytes.Basic Res. Cardiol.881993411420
Crossref | PubMed | ISI | Google Scholar
1132 SOHN D. H., KIM H. D.Effects of adenosine receptor agonists on volume-activated ion transport in pig red cells.J. Cell. Physiol.1461991318324
Crossref | PubMed | ISI | Google Scholar
1133 SOKABE M., SACHS F., JING Z.Quantitative video microscopy of patch clamped membranes: stress, strain, capacitance, and stretch channel activation.Biophys. J.591991722728
Crossref | PubMed | ISI | Google Scholar
1134 SOLC C. K., WINE J. J.Swelling-induced and depolarization-induced Cl channels in normal and cystic fibrosis epithelial cells.Am. J. Physiol.261(Cell Physiol. 30)1991C658C674
Link | Google Scholar
1135 SOLER C., FELIPE A., CASADO F. J., McGIVAN J. D., PASTOR-ANGLADA M.Hyperosmolarity leads to an increase in derepressed system A activity in the renal epithelial cell line NBL-1.Biochem. J.2891993653658
Crossref | PubMed | ISI | Google Scholar
1136 SOMA M. R., CORSINI A., PAOLETTI R.Cholesterol and mevalonic acid modulation in cell metabolism and multiplication.Toxicol. Lett.64–651992115
Crossref | ISI | Google Scholar
1137 SOMERO G. N.Protons, osmolytes, and fitness of internal milieu for protein function.Am. J. Physiol.251(Regulatory Integrative Comp. Physiol. 20)1986R197R213
Google Scholar
1138 SOMERO, G. N., C. B. OSMOND, and C. L. BOLIS. Water and Life: a Comparative Analysis of Water Relationships at the Organismic, Cellular, and Molecular Levels. Berlin: Springer-Verlag, 1992, p. 371.
Google Scholar
1139 SOROTA S.Swelling-induced chloride-sensitive current in canine atrial cells revealed by whole-cell patch-clamp method.Circ. Res.701992679687
Crossref | PubMed | ISI | Google Scholar
1140 SORRENTINO D., STUMP D. D., ZHOU S. L., VAN NESS K., ISOLA L. M., BERK P. D.The hepatocellular uptake of free fatty acids is selectively preserved during starvation.Gastroenterology107199414151424
Crossref | PubMed | ISI | Google Scholar
1141 SOUPART A., DECAUX G.Therapeutic recommendations for management of severe hyponatremia: current concepts on pathogenesis and prevention of neurologic complications.Clin. Nephrol.461996149169
PubMed | ISI | Google Scholar
1142 STAR R. A.Hyperosmolar states.Am. J. Med. Sci.3001990402412
Crossref | PubMed | ISI | Google Scholar
1143 STAR R. A., ZHANG B. X., LOESSBERG P. A., MUALLEM S.Regulatory volume decrease in the presence of HCO⁻₃ by single osteosarcoma cells UMR-106–01.J. Biol. Chem.26719921766517669
PubMed | ISI | Google Scholar
1144 STARKE L. C., JENNINGS M. L.K-Cl cotransport in rabbit red cells: further evidence for regulation by protein phosphatase type 1.Am. J. Physiol.264(Cell Physiol. 33)1993C118C124
Link | Google Scholar
1145 STAUB F., BAETHMANN A., PETERS J., KEMPSKI O.Glial cell volume and viability changes by lactacidosis.Acta Physiol. Scand.136198985
Google Scholar
1146 STAUB F., BAETHMANN A., PETERS J., WEIGT H., KEMPSKI O.Effects of lactacidosis on glial cell volume and viability.J. Cereb. Blood Flow Metab.101990866876
Crossref | PubMed | ISI | Google Scholar
1147 STAUB F., WINKLER A., PETERS J., KEMPSKI O., BAETHMANN A.Mechanisms of glial swelling by arachidonic acid.Acta Neurochir. Suppl.6019942023
PubMed | Google Scholar
1148 STAUB F., WINKLER A., PETERS J., KEMPSKI O., KACHEL V., BAETHMANN A.Swelling, acidosis, and irreversible damage of glial cells from exposure to arachidonic acid in vitro.J. Cereb. Blood Flow Metab.14199410301039
Crossref | PubMed | ISI | Google Scholar
1149 STAUB F., MACKERT B., KEMPSKI O., HABERSTOK J., PETERS J., BAETHMANN A.Schwellung und Schädigung von Nerven- und Gliazellen durch Azidose.Anasthesiol. Intensivmed. Notfallmed. Schmerzther.291994203209
Crossref | PubMed | Google Scholar
1150 STAUB F., MACKERT B., KEMPSKI O., PETERS J., BAETHMANN A.Swelling and death of neuronal cells by lactic acid.J. Neurol. Sci.11919937984
Crossref | PubMed | ISI | Google Scholar
1151 STAUB F., PETERS J., KEMPSKI O., SCHNEIDER G.-H., SCHÜRER L., BAETHMANN A.Swelling of glial cells in lactacidosis and by glutamate: significance of Cl⁻ transport.Brain Res.61019936974
Crossref | PubMed | ISI | Google Scholar
1152 STEENBERGEN J. M., BOHLEN H. G.Sodium hyperosmolarity of intestinal lymph causes arteriolar vasodilation in part mediated by EDRF.Am. J. Physiol.265(Heart Circ. Physiol. 34)1993H323H328
Google Scholar
1153 STEIDL M., RITTER M., LANG F.Regulation of potassium conductance by prostaglandins in cultured renal epitheloid (Madin-Darby canine kidney) cells.Pflügers Arch.4181991431436
Crossref | PubMed | ISI | Google Scholar
1155 STERNS R. H., BAER J., EBERSOL S., THOMAS D., LOHR J. W., KAMM D. E.Organic osmolytes in acute hyponatremia.Am. J. Physiol.264(Renal Fluid Electrolyte Physiol. 33)1993F833F836
Google Scholar
1156 STERNS R. H., RIGGS J. E., SCHOCHET S. S.Jr. Osmotic demyelination syndrome following correction of hyponatremia.N. Engl. J. Med.314198615351542
Crossref | PubMed | ISI | Google Scholar
1157 STERNS R. H., THOMAS D. J., HERNDON R. M.Brain dehydration and neurologic deterioration after rapid correction of hyponatremia.Kidney Int.3519896975
Crossref | PubMed | ISI | Google Scholar
1158 STEVENS M. J., HENRY D. N., THOMAS T. P., KILLEN P. D., GREENE D. A.Aldose reductase gene expression and osmotic dysregulation in cultured human retinal pigment epithelial cells.Am. J. Physiol.265(Endocrinol. Metab. 28))1993E428F438
Google Scholar
1159 STOLL B., GEROK W., LANG F., HÄUSSINGER D.Liver cell volume and protein synthesis.Biochem. J.2871992217222
Crossref | PubMed | ISI | Google Scholar
1160 STOREY K. B., STOREY J. M.Freeze tolerance in animals.Physiol. Rev.6819882784
Link | ISI | Google Scholar
1161 STOSSEL T. P.From signal to pseudopod. How cells control cytoplasmic actin assembly.J. Biol. Chem.26419891826118264
PubMed | ISI | Google Scholar
1162 STOSSEL T. P.On the crawling of animal cells.Science260199310861094
Crossref | PubMed | ISI | Google Scholar
1164 STRANGE K.Ouabain-induced cell swelling in rabbit cortical collecting tubule: NaCl transport by principal cells.J. Membr. Biol.1071989249261
Crossref | PubMed | ISI | Google Scholar
1165 STRANGE K.Volume regulatory Cl⁻ loss after Na⁺ pump inhibition in CCT principal cells.Am. J. Physiol.260(Renal Fluid Electrolyte Physiol. 29)1991F225F234
Google Scholar
1166 STRANGE K.Regulation of solute and water balance and cell volume in the central nervous system.J. Am. Soc. Nephrol.319921227
PubMed | ISI | Google Scholar
1167 STRANGE K.Maintenance of cell volume in the central nervous system.Pediatr. Nephrol.71993689697
Crossref | PubMed | ISI | Google Scholar
1168 STRANGE, K. (Editor). Cellular and Molecular Physiology of Cell Volume Regulation. Boca Raton, FL: CRC, 1994.
Google Scholar
1169 STRANGE K., JACKSON P. S.Swelling-activated organic osmolyte efflux: a new role for anion channels.Kidney Int.4819959941003
Crossref | PubMed | ISI | Google Scholar
1170 STRANGE K., MORRISON R.Volume regulation during recovery from chronic hypertonicity in brain glial cells.Am. J. Physiol.263(Cell Physiol. 32)1992C412C419
Link | Google Scholar
1171 STRANGE K., MORRISON R., SHRODE L., PUTNAM R.Mechanism and regulation of swelling-activated inositol efflux in brain glial cells.Am. J. Physiol.265(Cell Physiol. 34)1993C244C256
Link | Google Scholar
1172 STRUPP M., STAUB F., GRAFE P.A Ca²⁺- and pH-dependent K⁺ channel of rat C6 glioma cells and its possible role in acidosis-induced cell swelling.Glia91993136145
Crossref | PubMed | ISI | Google Scholar
1173 SULEYMANIAN M. A., CLEMO H. F., COHEN N. M., BAUMGARTEN C. M.Stretch-activated channel blockers modulate cell volume in cardiac ventricular myocytes.J. Mol. Cell. Cardiol.271995721728
Crossref | PubMed | ISI | Google Scholar
1174 SULLIVAN L. P., WALLACE D. P., CLANCY R. L., LECHENE C., GRANTHAM J. J.Cellular electrolyte and volume changes induced by acidosis in the rabbit proximal straight tubule.J. Am. Soc. Nephrol.2199110301040
PubMed | ISI | Google Scholar
1175 SULLIVAN L. P., WALLACE D. P., CLANCY R. L., LECHENE C., GRANTHAM J. J.Effect of cellular acidosis on cell volume in S2 segments of renal proximal tubules.Am. J. Physiol.258(Renal Fluid Electrolyte Physiol. 27)1990F831F839
Google Scholar
1176 SULLIVAN L. P., WALLACE D. P., GRANTHAM J. J.Coupling of cell volume and membrane potential changes to fluid secretion in a model of renal cysts.Kidney Int.45199413691380
Crossref | PubMed | ISI | Google Scholar
1177 SUN A. M., HEBERT S. C.Rapid hypertonic cell volume regulation in the perfused inner medullary collecting duct.Kidney Int.361989831842
Crossref | PubMed | ISI | Google Scholar
1178 SUN, A. M., and S. C. HEBERT. Volume regulation in renal medullary nephron segments. In: Cellular and Molecular Physiology of Cell Volume Regulation, edited by K. Strange. Boca Raton, FL: CRC, 1994, p. 49–62.
Google Scholar
1179 SUN A. M., GROSSMAN E. B., LOMBARDI M., HEBERT S. C.Vasopressin alters the mechanism of apical Cl entry from Na:Cl to Na:K:2Cl cotransport in mouse medullary thick ascending limb.J. Membr. Biol.12019918394
Crossref | PubMed | ISI | Google Scholar
1180 SUZUKI M., KAWAHARA K., OGAWA A., MORITA T., KAWAGUCHI Y., KURIHARA S., SAKAI O.[Ca²⁺]_i rises via G protein during regulatory volume decrease in rabbit proximal tubule cells.Am. J. Physiol.258(Renal Fluid Electrolyte Physiol. 27)1990F690F696
Google Scholar
1181 SUZUKI Y., OHTSUYAMA M., SAMMAN G., SATA F., SATO K.Ionic basis of methacholine-induced shrinkage of dissociated eccrine clear cells.J. Membr. Biol.12319913341
Crossref | PubMed | ISI | Google Scholar
1182 SWEEZEY N. B., GAUTHIER C., GAGNON S., FERRETTI E., KOPELMAN H.Progesterone and estradiol inhibit CFTR mediated ion transport by pancreatic epithelial cells.Am. J. Physiol.271(Gastrointest. Liver Physiol. 34)1996G747G754
Google Scholar
1183 SZABO I., GULBINS E., APFEL H., ZHANG X., BARTH P., BUSCH A. E., SCHLOTTMANN K., PONGS O., LANG F.Tyrosine-phosphorylation dependent suppression of a voltage-gated K⁺ channel in T-Lymphocytes upon Fas-stimulation.J. Biol. Chem.27119962046520469
Crossref | PubMed | ISI | Google Scholar
1184 TAGA K., CHRETIEN J., CHERNEY B., DIAZ L., BROWN M., TOSATO G.Interleukin-10 inhibits apoptotic cell death in infectious mononucleosis T cells.J. Clin. Invest.941994251260
Crossref | PubMed | ISI | Google Scholar
1185 TAKAHASHI A., YAMAGUCHI H., MIYAMOTO H.Change in K⁺ current of HeLa cells with progression of the cell cycle studied by patch-clamp technique.Am. J. Physiol.265(Cell Physiol. 34)1993C328C336
Link | Google Scholar
1186 TAKAHASHI K., MATSUMOTO T., KUBO S., HARAOKA M., TANAKA M., KUMAZAWA J.Influence of hyperosmotic environment comparable to the renal medulla upon membrane NADPH oxidase of human polymorphonuclear leukocytes.J. Urol.152199416221625
Crossref | PubMed | ISI | Google Scholar
1187 TAKAHASHI K., MATSUMOTO T., OGATA N., MIZUNOE Y., TANAKA M., KUMAZAWA J.Direct inactivation of human polymorphonuclear leukocyte by hyperosmotic urea comparable to the renal medulla.J. Urol.1491993386389
Crossref | PubMed | ISI | Google Scholar
1188 TAKEDA M., HOMMA T., BREYER M. D., HORIBA N., HOOVER R. L., KAWAMOTO S., ICHIKAWA I., KON V.Volume and agonist-induced regulation of myosin light-chain phosphorylation in glomerular mesangial cells.Am. J. Physiol.264(Renal Fluid Electrolyte Physiol. 33)1993F421F426
Google Scholar
1189 TAKEMURA T., SATO F., SAGA K., SUZUKI Y., SATO K.Intracellular ion concentrations and cell volume during cholinergic stimulation of eccrine secretory coil cells.J. Membr. Biol.1191991211219
Crossref | PubMed | ISI | Google Scholar
1190 TAKENAKA M., BAGNASCO S. M., PRESTON A. S., UCHIDA S., YAMAUCHI A., KWON H. M., HANDLER J. S.The canine betaine gamma-amino-n-butyric acid transporter gene: diverse mRNA isoforms are regulated by hypertonicity and are expressed in a tissue-specific manner.Proc. Natl. Acad. Sci. USA92199510721076
Crossref | PubMed | ISI | Google Scholar
1191 TAKENAKA M., PRESTON A. S., KWON H. M., HANDLER J. S.The tonicity-sensitive element that mediates increased transcription of the betaine transporter gene in response to hypertonic stress.J. Biol. Chem.26919942937929381
PubMed | ISI | Google Scholar
1192 TANAKA K., JAY G., ISSELBACHER K. J.Expression of heat-shock and glucose-regulated genes: differential effects of glucose starvation and hypertonicity.Biochim. Biophys. Acta9501988138146
Crossref | PubMed | ISI | Google Scholar
1193 TANEJA S., AHMAD F.Increased thermal stability of proteins in the presence of amino acids.Biochem. J.3031994147153
Crossref | PubMed | ISI | Google Scholar
1194 TANIGUCHI J., GUGGINO W. B.Membrane stretch: a physiological stimulator of Ca²⁺-activated K⁺ channels in thick ascending limb.Am. J. Physiol.257(Renal Fluid Electrolyte Physiol. 26)1989F347F352
Google Scholar
1195 TARTERA C., METCALF E. S.Osmolarity and growth phase overlap in regulation of Salmonella typhi adherence to and invasion of human intestinal cells.Infect. Immun.61199330843089
PubMed | ISI | Google Scholar
1196 TAWATA M., OHTAKA M., HOSAKA Y., ONAYA T.Aldose reductase mRNA expression and its activity are induced by glucose in fetal rat aortic smooth muscle (A10) cells.Life Sci.511992719726
Crossref | PubMed | ISI | Google Scholar
1197 TERADA Y., TOMITA K., HOMMA M. K., NONOGUCHI H., YANG T., YAMADA T., YUASA Y., KREBS E. G., SASAKI S., MARUMO F.Sequential activation of Raf-1 kinase, mitogen-activated protein (MAP), kinase kinase, MAP kinase, and S6 kinase by hyperosmolality in renal cells.J. Biol. Chem.26919943129631301
PubMed | ISI | Google Scholar
1198 TERUBAYASHI H., SATO S., NISHIMURA C., KADOR P. F., KINOSHITA J. H.Localization of aldose and aldehyde reductase in the kidney.Kidney Int.361989843851
Crossref | PubMed | ISI | Google Scholar
1199 TEULON J., RONCO P. M., GENITEAU-LEGENDRE M., BAUDOUIN B., ESTRADE S., CASSINGENA R., VANDEWALLE A.Transformation of renal tubule epithelial cells by simian virus 40 is associated with emergence of Ca²⁺-insensitive K⁺ channels and altered mitogenic sensitivity to K⁺ channel blockers.J. Cell. Physiol.1511992113125
Crossref | PubMed | ISI | Google Scholar
1200 THAKAR M., BILENKO A., BECKTEL W. J.Osmolyte mediation of T7 DNA polymerase and plasmid DNA stability.Biochemistry3319941225512259
Crossref | PubMed | ISI | Google Scholar
1201 THATTE H. S., KASSCHAU M. R., FURLONG S. T., BYAM-SMITH M. P., WILLIAMS D. F., GOLAN D. E.Schistosoma mansoni: membranes from adult worms reversibly perturb shape, volume, and membrane organization of intact human red blood cells.Exp. Parasitol.7619931322
Crossref | PubMed | ISI | Google Scholar
1202 THEODOROPOULOS P. A., STOURNARAS C., STOLL B., MARKOGIANNAKIS E., LANG F., GRAVANIS A., HÄUSSINGER D.Hepatocyte swelling leads to rapid decrease of the G-/total actin ratio and increases actin mRNA levels.FEBS Lett.3111992241245
Crossref | PubMed | ISI | Google Scholar
1203 THIEMANN A., GRÜNDER S., PUSCH M., JENTSCH T. J.A chloride channel widely expressed in epithelial and non-epithelial cells.Nature35619925760
Crossref | PubMed | ISI | Google Scholar
1204 THOMAS-YOUNG R. J., SMITH T. C., LEVINSON C.Regulatory volume decrease in Ehrlich ascites tumor cells is not mediated by a rise in intracellular calcium.Biochim. Biophys. Acta114619938186
Crossref | PubMed | ISI | Google Scholar
1205 THOMPSON A. A., CORNELIUS A. S., ASAKURA T., HORIUCHI K.Comparative studies of phenothiazine derivatives for their effects on swelling of normal and sickle erythrocytes.Gen. Pharmacol.2419939991006
Crossref | PubMed | Google Scholar
1206 THORNHILL W. B., LARIS P. C.KCl loss and cell shrinkage in the Ehrlich ascites tumour cell induced by hypotonic media, 2-deoxyglucose and propanolol.Biochim. Biophys. Acta7731984207218
Crossref | PubMed | ISI | Google Scholar
1207 THOROED S. M., FUGELLI K.Free amino compounds and cell volume regulation in erythrocytes from different marine fish species under hypoosmotic conditions: the role of a taurine channel.J. Comp. Physiol. B Biochem. Syst. Environ. Physiol.1641994110
Crossref | ISI | Google Scholar
1208 THURSTON J. H., SHERMAN W. R., HAUHART R. E., KLOEPPER R. F.Myo-inositol: a newly identified nonnitrogenous osmoregulatory molecule in mammalian brain.Pediatr. Res.261989482485
Crossref | PubMed | ISI | Google Scholar
1209 TILLY B. C., EDIXHOVEN M. J., TERTOOLEN L. G. J., MORII N., SAITO Y., NARUMIYA S., DE JONGE H. R.Activation of the osmo-sensitive chloride conductance involves the p21^rho and is accompanied by a transient reorganization of the F-actin cytoskeleton.Mol. Biol. Cell7199614191427
Crossref | PubMed | ISI | Google Scholar
1210 TILLY B. C., EDIXHOVEN M. J., VAN DEN BERGHE N., BOT A. G. M., DE JONGE H. R.Ca²⁺-mobilizing hormones potentiate hypotonicity-induced activation of ionic conductances in intestine 407 cells.Am. J. Physiol.267(Cell Physiol. 36)1994C1271C1278
Link | Google Scholar
1211 TILLY B. C., VAN DEN BERGHE N., TERTOOLEN L. G. J., EDIXHOVEN M. J., DE JONGE H. R.Protein tyrosine phosphorylation is involved in osmoregulation of ionic conductances.J. Biol. Chem.26819931991919922
PubMed | ISI | Google Scholar
1212 TILNEY L. G., INOUE S.Acrosomal reaction of Thyone sperm. II. The kinetics and possible mechanism of acrosomal process elongation.J. Cell Biol.931982820827
Crossref | PubMed | ISI | Google Scholar
1213 TINEL E., WEHNER F., KINNE R. K. H.Arachidonic acid as a second messenger for hypotonicity induced calcium transient rat IMCD cells.Pflügers Arch.4331997245253
Crossref | PubMed | ISI | Google Scholar
1214 TOBEY N. A., CRAGOE E. J., ORLANDO R. C.HCl-induced cell edema in rabbit esophageal epithelium: a bumetanide-sensitive process.Gastroenterology1091995414421
Crossref | PubMed | ISI | Google Scholar
1215 TOHYAMA Y., KAMEJI T., HAYASHI S.Mechanisms of dramatic fluctuations of ornithine decarboxylase activity upon tonicity changes in primary cultured rat hepatocytes.Eur. J. Biochem.202199113271331
Crossref | PubMed | Google Scholar
1216 TOKIWA G., DIKIC I., LEV S., SCHLESINGER J.Activation of Pyk2 by stress signals and coupling with JNK signaling pathway.Science2731996792794
Crossref | PubMed | ISI | Google Scholar
1217 TOMINAGA M., TOMINAGA T., MIWA A., OKADA Y.Volume-sensitive chloride channel activity does not depend on endogenous P-glycoprotein.J. Biol. Chem27019952788727893
Crossref | PubMed | ISI | Google Scholar
1218 TOMLINSON D. R., STEVENS E. J., DIEMEL L. T.Aldose reductase inhibitors and their potential for the treatment of diabetic complications.Trends. Pharmacol. Sci.151994293297
Crossref | PubMed | ISI | Google Scholar
1219 TORCHIA, J., C. LYTLE, D. J. PON, B. FORBUSH III, and A. K. SEN. The Na-K-Cl cotransporter of avian salt gland. Phosphorylation in response to cAMP-dependent and calcium-dependent secretagogues. J. Biol. Chem. 267: 25444–25450, 1992.
Google Scholar
1220 TRACHTMAN H.Cell volume regulation: a review of cerebral adaptive mechanisms and implications for clinical treatment of osmolal disturbances: I.Pediatr. Nephrol.51991743750
Crossref | PubMed | ISI | Google Scholar
1221 TRACHTMAN H.Cell volume regulation: a review of cerebral adaptive mechanisms and implications for clinical treatment of osmolal disturbances: II.Pediatr. Nephrol.61992104112
Crossref | PubMed | ISI | Google Scholar
1222 TRACHTMAN H., FUTTERWEIT S., STURMAN J. A.Cerebral taurine transport is increased during streptozocin-induced diabetes in rats.Diabetes41199211301140
Crossref | PubMed | ISI | Google Scholar
1223 TRACHTMAN H., FUTTERWEIT S., TONIDANDEL W., GULLANS S. R.The role of organic osmolytes in the cerebral cell volume regulatory response to acute and chronic renal failure.J. Am. Soc. Nephrol.3199319131919
PubMed | ISI | Google Scholar
1224 TRAYNELIS S. F., DINGLEDINE R.Role of extracellular space in hyperosmotic suppression of potassium-induced electrographic seizures.J. Neurophysiol.611989927938
Link | ISI | Google Scholar
1225 TREZISE A. E., ROMANO P. R., GILL D. R., HYDE S. C., SEPULVEDA F. V., BUCHWALD M., HIGGINS C. F.The multidrug resistance and cystic fibrosis genes have complementary patterns of epithelial expression.EMBO J.11199242914303
Crossref | PubMed | ISI | Google Scholar
1226 TRUMP B. F., BEREZESKY I. K.Calcium-mediated cell injury and cell death.FASEB J.91995219228
Crossref | PubMed | ISI | Google Scholar
1227 TSENG G. N.Cell swelling increases membrane conductance of canine cardiac cells: evidence for a volume-sensitive Cl channel.Am. J. Physiol.262(Cell Physiol. 31)1992C1056C1068
Link | Google Scholar
1228 TSUMURA T., OIKI S., UEDA S., OKUMA M., OKADA Y.Sensitivity of volume sensitive Cl conductance in human epithelial cells to extracellular nucleotides.Am. J. Physiol.271(Cell Physiol. 40)1996C1872C1878
Link | Google Scholar
1229 TURNER D. A., AITKEN P. G., SOMJEN G. G.Optical mapping of translucence changes in rat hippocampal slices during hypoxia.Neurosci. Lett.1951995209213
Crossref | PubMed | ISI | Google Scholar
1230 TURNHEIM K.Epithelial sodium transport: basic autoregulatory mechanisms.Physiol. Res.431994211218
PubMed | ISI | Google Scholar
1231 TURNHEIM K.Intrinsic regulation of apical sodium entry in epithelia.Physiol. Rev.711991429445
Link | ISI | Google Scholar
1232 TURNHEIM K., FRIZZELL R. A., SCHULTZ S. G.Interaction between cell sodium and the amiloride-sensitive sodium entry step in rabbit colon.J. Membr. Biol.391978233256
Crossref | PubMed | ISI | Google Scholar
1233 TURNHEIM K., THOMPSON S. M., SCHULTZ S. G.Relation between intracellular sodium and active sodium transport in rabbit colon: current-voltage relations of the apical sodium entry mechanism in the presence of varying luminal sodium concentrations.J. Membr. Biol.761983299309
Crossref | PubMed | ISI | Google Scholar
1234 UBL J., MURER H., KOLB H.-A.Hypotonic shock evokes opening of Ca²⁺-activated K channels in opossum kidney cells.Pflügers Arch.4121988551553
Crossref | PubMed | ISI | Google Scholar
1235 UBL J., MURER H., KOLB H.-A.Ion channels activated by osmotic and mechanical stress in membranes of opossum kidney cells.J. Membr. Biol.1041988223232
Crossref | PubMed | ISI | Google Scholar
1236 UCHIDA S., GARCIA-PEREZ A., MURPHY H., BURG M.Signal for induction of aldose reductase in renal medullary cells by high external NaCl.Am. J. Physiol.256(Cell Physiol. 25)1989C614C620
Link | Google Scholar
1237 UCHIDA S., GREEN N., COON H., TRICHE T., MIMS S., BURG M.High NaCl induces stable changes in phenotype and karyotype of renal cells in culture.Am. J. Physiol.253(Cell Physiol. 22)1987C230C242
Link | Google Scholar
1238 UCHIDA S., KWON H. M., PRESTON A. S., HANDLER J. S.Expression of Madin-Darby canine kidney cell Na⁺- and Cl⁻-dependent taurine transporter in Xenopus laevis oocytes.J. Biol. Chem.266199196059609
PubMed | ISI | Google Scholar
1239 UCHIDA S., KWON H. M., YAMAUCHI A., PRESTON A. S., MARUMO F., HANDLER J. S.Molecular cloning of the cDNA for an MDCK cell Na⁺- and Cl⁻-dependent taurine transporter that is regulated by hypertonicity.Proc. Natl. Acad. Sci. USA89199282308234
Crossref | PubMed | ISI | Google Scholar
1240 UCHIDA S., NAKANISHI T., KWON H. M., PRESTON A. S., HANDLER J. S.Taurine behaves as an osmolyte in Madin-Darby canine kidney cells. Protection by polarized, regulated transport of taurine.J. Clin. Invest.881991656662
Crossref | PubMed | ISI | Google Scholar
1241 UCHIDA S., SASAKI S., FURUKAWA T., HIRAOKA M., IMAI T., HIRATA Y., MARUMO F.Molecular cloning of a chloride channel that is regulated by dehydration and expressed predominantly in kidney medulla.J. Biol. Chem.268199338213824
PubMed | ISI | Google Scholar
1242 UCHIDA S., YAMAUCHI A., PRESTON A. S., KWON H. M., HANDLER J. S.Medium tonicity regulates expression of the Na⁺- and Cl⁻-dependent betaine transporter in Madin-Darby canine kidney cells by increasing transcription of the transporter gene.J. Clin. Invest.91199316041607
Crossref | PubMed | ISI | Google Scholar
1243 ULLRICH K. J.Glycerylphosphorylcholinumsatz und Glycerylphosphorylcholindiesterase in der Säugetier-Niere.Biochem. Z.331195998102
Google Scholar
1244 URBAN J. P. G., HALL A. C., GEHL K. A.Regulation of matrix synthesis rates by the ionic and osmotic environment of articular chondrocytes.J. Cell. Physiol.1541993262270
Crossref | PubMed | ISI | Google Scholar
1245 USSING H. H.Volume regulation of frog skin epithelium.Acta Physiol. Scand.1141982363369
Crossref | PubMed | Google Scholar
1246 USSING, H. H. Volume regulation of frog skin epithelium. In: Comparative Physiology. Cell Volume Regulation, edited by K. W. Beyenbach. Basel: Karger, 1990, vol. 4, p. 87–113.
Google Scholar
1247 UYESAKA N., HASEGAWA S., ISHIOKA N., ISHIOKA R., SHIO H., SCHECHTER A. N.Effects of superoxide anions on red cell deformability and membrane proteins.Biorheology291992217229
Crossref | PubMed | ISI | Google Scholar
1248 VAIRO G., ROYSTON A. K., HAMILTON J. A.Biochemical events accompanying macrophage activation and the inhibition of colony-stimulating factor-1-induced macrophage proliferation by tumor necrosis factor-alpha, interferon-gamma and lipopolysaccharide.J. Cell. Physiol.1511992630641
Crossref | PubMed | ISI | Google Scholar
1249 VALVERDE M. A., BOND T. D., HARDY S. P., TAYLOR J. C., HIGGINS C. F., ALTAMIRANO J., ALVAREZ-LEEFMANS F. J.The multidrug resistance P glycoprotein modulates cell regulatory volume decrease.EMBO J.15199644604468
Crossref | PubMed | ISI | Google Scholar
1250 VALVERDE M. A., DIAZ M., SEPULVEDA F. V., GILL D. R., HYDE S. C., HIGGINS C. F.Volume-regulated chloride channels associated with the human multidrug-resistant P-glycoprotein.Nature3551992830833
Crossref | PubMed | ISI | Google Scholar
1251 VALVERDE M. A., O'BRIEN J. A., SEPULVEDA F. V., RATCLIFF R., EVANS M. J., COLLEDGE W. H.Inactivation of the murine cftr gene abolishes cAMP-mediated but not Ca²⁺-mediated secretagogue-induced volume decrease in small-intestinal crypts.Pflügers Arch.4251993434438
Crossref | PubMed | ISI | Google Scholar
1252 VALVERDE M. A., O'BRIEN J. A., SEPULVEDA F. V., RATCLIFF R. A., EVANS M. J., COLLEDGE W. H.Impaired cell volume regulation in intestinal crypt epithelia of cystic fibrosis mice.Proc. Natl. Acad. Sci. USA92199590389041
Crossref | PubMed | ISI | Google Scholar
1253 VANDENBERG J. I., YOSHIDA A., KIRK K., POWELL T.Swelling-activated and isoprenaline-activated chloride currents in guinea pig cardiac myocytes have distinct electrophysiology and pharmacology.J. Gen. Physiol.10419949971017
Crossref | PubMed | ISI | Google Scholar
1254 VANDEN BROECK, J., A. DE LOOF, and P. CALLAERTS. Electrical-ionic control of gene expression. Int. J. Biochem. 24: 1907–1916, 1992.
Google Scholar
1255 VAN DER MEULEN J. A., KLIP A., GRINSTEIN S.Possible mechanism for cerebral edema in diabetic ketoacidosis.Lancet21987306308
Crossref | PubMed | ISI | Google Scholar
1256 VANDEWALLE A., VUILLEMIN T., TEULON J., BOUDOUIN B., WAHBE F., BENS M., CASSINGENA R., RONCO P.K⁺ fluxes mediated by Na⁺/K⁺/Cl⁻ cotransport and Na⁺/K⁺-ATPase pumps in renal tubule cell lines transformed by wild-type and temperature-sensitive strains of simian virus 40.J. Cell. Physiol.1541993466477
Crossref | PubMed | ISI | Google Scholar
1257 VAN ROSSUM G. D. V., ERNST S. A., RUSSO M. A.Relative effects of furosemide and ethacrynic acid on ion transport and energy metabolism in slices of rat kidney cortex.Naunyn-Schmiedebergs Arch. Pharmacol.31719819096
Crossref | PubMed | ISI | Google Scholar
1258 VAN ROSSUM G. D. V., RUSSO M. A.Ouabain-resistant mechanism of volume control and the ultrastructural organization of liver slices recovering from swelling in vitro.J. Membr. Biol.591981191209
Crossref | PubMed | ISI | Google Scholar
1259 VAN ROSSUM G. D. V., RUSSO M. A.Requirement of Cl⁻ and Na⁺ for the ouabain-resistant control of cell volume in slices of rat liver.J. Membr. Biol.7719846376
Crossref | PubMed | ISI | Google Scholar
1260 VAN ROSSUM G. D. V., RUSSO M. A., SCHISSELBAUER J. C.Role of cytoplasmic vesicles in volume maintenance.Curr. Top. Membr. Transp.3019874574
Crossref | ISI | Google Scholar
1261 VAN SCHAFTINGEN E., VANDERCAMMEN A.Mechanism of the stimulatory effect of a potassium rich medium on the phosphorylation of glucose in isolated rat hepatocytes.Eur. J. Biochem.2041992363369
Crossref | PubMed | Google Scholar
1262 VAUTRIN J., KRIEBEL M. E.Characteristics of slow-miniature endplate currents show a subunit composition.Neuroscience4119917188
Crossref | PubMed | ISI | Google Scholar
1263 VENOSA R. A.Hypo-osmotic stimulation of active Na⁺ transport in frog muscle: apparent upregulation of Na⁺ pumps.J. Membr. Biol.120199197104
Crossref | PubMed | ISI | Google Scholar
1264 VERBALIS J. G.Hyponatremia: epidemiology, pathophysiology, and therapy.Curr. Opin. Nephrol. Hypertens.21993636652
Crossref | PubMed | Google Scholar
1265 VERBALIS J. G., DRUTAROSKY M. D.Adaptation to chronic hypoosmolality in rats.Kidney Int.341988351360
Crossref | PubMed | ISI | Google Scholar
1266 VERBALIS J. G., GULLANS S. R.Hyponatremia causes large sustained reductions in brain content of multiple organic osmolytes in rats.Brain Res.5671991274282
Crossref | PubMed | ISI | Google Scholar
1267 VERHEUL H. B., BALAZS R., BERKELBACH J. W.VAN DER SPRENKEL, C. A. TULLEKEN, K. NICOLAY, and M. VAN LOOKEREN CAMPAGNE. Temporal evolution of NMDA-induced excitoxicity in the neonatal rat brain measured with ¹H nuclear magnetic resonance imaging.Brain Res.6181993203212
Crossref | PubMed | ISI | Google Scholar
1268 VERNACE M. A., MENTO P. F., MAITA M. E., GIRARDI E. P., CHANG M. D., NORD E. P., WILKES B. M.Osmolar regulation of endothelin in rat renal medullary interstitial cells.J. Clin. Invest.961995183191
Crossref | PubMed | ISI | Google Scholar
1269 VIANA F., VAN ACKER K., DE GREEF C., EGGERMONT J., RAEYMAEKERS L., DROOGMANS G., NILIUS B.Drug-transport and volume-activated chloride channel functions in human erythroleukemia cells: relation to expression level of P-glycoprotein.J. Membr. Biol.14519958798
Crossref | PubMed | ISI | Google Scholar
1270 VIDEEN J. S., MICHAELIS T., PINTO P., ROSS B. D.Human cerebral osmolytes during chronic hyponatremia. A proton magnet resonance spectroscopy study.J. Clin. Invest.951995788793
Crossref | PubMed | ISI | Google Scholar
1271 VIEYRA A., CARUSO-NEVES C.Interactions of the regulatory ligands Mg²⁺ and MgATP²⁻ with the renal plasma membrane Ca²⁺-ATPase: effects of osmolytes that stabilize or destabilize protein structure.Braz. J. Med. Biol. Res.261993373381
PubMed | ISI | Google Scholar
1272 VIEYRA A., CARUSO-NEVES C., MEYER-FERNANDES J. R.ATP in equilibrium with ³²P_i exchange catalyzed by plasma membrane Ca²⁺-ATPase from kidney proximal tubules.J. Biol. Chem.26619911032410330
PubMed | ISI | Google Scholar
1273 VILLAZ M., CINNINGER J. C., MOODY W. J.A voltage-gated chloride channel in ascidian embryos modulated by both the cell cycle clock and cell volume.J. Physiol. (Lond.)4881995689699
Crossref | Google Scholar
1274 VILLEREAL M. L., MIX-MULDOON L. L., VICENTINI L. M., JAMIESON G. A.Jr., and N. E. OWEN. Mechanisms of growth factor stimulation of Na⁺/H⁺ exchange in cultured fibroblasts.Curr. Top. Membr. Transp.261986175192
Crossref | ISI | Google Scholar
1275 VINIEGRA S., CRAGOE E. J.Jr., and C. A. RABITO. Heterogeneity of the Na⁺/H⁺ antiport systems in renal cells.Biochim. Biophys. Acta1106199299109
Crossref | PubMed | ISI | Google Scholar
1276 VITOUX D., OLIVIERI O., GARAY R. P., CRAGOE E. J.Jr., F. GALACTEROS, and Y. BEUZARD. Inhibition of K⁺ efflux and dehydration of sickle cells by [(dihydroindenyl)oxy]alkanoic acid: an inhibitor of the K⁺Cl⁻ cotransport system.Proc. Natl. Acad. Sci. USA86198942734276
Crossref | PubMed | ISI | Google Scholar
1277 VOLK K. A., ZHANG C., HUSTED R. F., STOKES J. B.Cl current in IMCD cells activated by hypotonicity: time course, ATP dependence, and inhibitors.Am. J. Physiol.271(Renal Fluid Electrolyte Physiol. 40)1996F552F559
Google Scholar
1278 VOLK T., FRÖMTER E., KORBMACHER C.Hypertonicity activates nonselective cation channels in mouse cortical collecting duct cells.Proc. Natl. Acad. Sci. USA92199584788482
Crossref | PubMed | ISI | Google Scholar
1279 VÖLKL H., BUSCH G. L., HÄUSSINGER D., LANG F.Alkalinization of acidic cellular compartments following cell swelling.FEBS Lett.33819942730
Crossref | PubMed | ISI | Google Scholar
1280 VÖLKL H., FRIEDRICH F., HÄUSSINGER D., LANG F.Effect of cell volume on Acridine Orange fluorescence in hepatocytes.Biochem. J.29519931114
Crossref | PubMed | ISI | Google Scholar
1281 VÖLKL H., LANG F.Ionic requirement for regulatory cell volume decrease in renal straight proximal tubules.Pflügers Arch.412198816
Crossref | PubMed | ISI | Google Scholar
1282 VÖLKL H., LANG F.Effect of potassium on cell volume regulation in renal straight proximal tubules.J. Membr. Biol.1171990113122
Crossref | PubMed | ISI | Google Scholar
1283 VÖLKL H., REHWALD W., WAITZ W., HÄUSSINGER D., LANG F.Acridine Orange fluorescence in renal proximal tubules: effects of NH₃/NH⁺₄ and cell volume.Cell. Physiol. Biochem.319932833
Crossref | ISI | Google Scholar
1284 VOM DAHL, S., B. STOLL, W. GEROK, and D. HÄUSSINGER. Inhibition of proteolysis by cell swelling in the liver requires intact microtubular structures. Biochem. J. 308: 529–536, 1995.
Google Scholar
1285 VOM DAHL, S., and D. HÄUSSINGER. Nutritional state and the swelling-induced inhibition of proteolysis in the perfused rat liver. J. Nutr. 126: 395–402, 1996.
Google Scholar
1286 VOM DAHL, S., C. HALLBRUCKER, F. LANG, and D. HÄUSSINGER. Regulation of cell volume in the perfused rat liver by hormones. Biochem. J. 280: 105–109, 1991.
Google Scholar
1287 VOM DAHL, S., C. HALLBRUCKER, F. LANG, W. GEROK, and D. HÄUSSINGER. Regulation of liver cell volume and proteolysis by glucagon and insulin. Biochem. J. 278: 771–777, 1991.
Google Scholar
1288 VOM DAHL, S., C. HALLBRUCKER, F. LANG, and D. HÄUSSINGER. Role of eicosanoids, inositol phosphates and extracellular Ca²⁺ in cell volume regulation of rat liver. Eur. J. Biochem. 198: 73–83, 1991.
Google Scholar
1289 VON HARSDORF R., LANG R., FULLERTON M., SMITH A. I., WOODCOCK E. A.Right atrial dilation increases inositol-(1,4,5) trisphosphate accumulation. Implications for the control of atrial natriuretic peptide release.FEBS Lett.2331988201205
Crossref | PubMed | ISI | Google Scholar
1290 WAITE M. R. F., PFEFFERKORN E. R.Effect of altered osmotic pressure on the growth of Sindbis virus.J. Virol.21968759760
PubMed | ISI | Google Scholar
1291 WAKABAYASHI S., BERTRAND B., IKEDA T., POUYSSÉGUR J., SHIGEKAWA M.Mutation of calmodulin-binding site renders the Na⁺/H⁺ exchanger (NHE1) highly H⁺-sensitive and Ca²⁺ regulation-defective.J. Biol. Chem.26919941371013715
Crossref | PubMed | ISI | Google Scholar
1292 WAKABAYASHI, S., P. FAFOURNOUX, C. SARDET, and J. POUYSSÉGUR. The Na⁺/H⁺ antiporter cytoplasmic domain mediates growth factor signals and controls “H⁺-sensing.” Proc. Natl. Acad. Sci. USA 89: 2424–2428, 1992.
Google Scholar
1293 WAKABAYASHI S., SARDET C., FAFOURNOUX P., COUNILLON L., MELOCHE S., PAGES G., POUYSSEGUR J.Structure function of the growth-factor-activatable Na⁺/H⁺ exchanger (NHE1).Rev. Physiol. Biochem. Pharmacol.1191992157186
PubMed | ISI | Google Scholar
1294 WAKABAYASHI S., SHIGEKAWA M., POUYSSEGUR J.Molecular physiology of vertebrate Na⁺/H⁺ exchangers.Physiol. Rev.7719975174
Link | ISI | Google Scholar
1295 WALDEGGER S., BARTH P., RABER G., LANG F.Cloning and characterization of a putative human serine/theonine protein kinase transcriptionally modified during anisotonic and isotonic alterations of cell volume.Proc. Natl. Acad. Sci. USA94199744404445
Crossref | PubMed | ISI | Google Scholar
1296 WALDEGGER S., PINGGERA G., KLOIBER K., RITTER M., WÖLL E., HUMPELER E., MALY K., GRUNICKE H., LANG F.Further studies on the nature of cell membrane potential oscillations in NIH-3T3 fibroblasts expressing the ras oncogene.Cell. Physiol. Biochem.319938996
Crossref | ISI | Google Scholar
1297 WALTERS R. J., O'BRIEN J. A., VALVERDE M. A., SEPULVEDA F. V.Membrane conductance and cell volume changes evoked by vasoactive intestinal polypeptide and carbachol in small intestinal crypts.Pflügers Arch.4211992598605
Crossref | PubMed | ISI | Google Scholar
1298 WALZ W.Role of Na/K/Cl cotransport in astrocytes.Can. J. Physiol. Pharmacol.70, Suppl.1992S260S262
Crossref | PubMed | ISI | Google Scholar
1299 WALZ W., MUKERJI S.Simulation of aspects of ischemia in cell culture: changes in lactate compartmentation.Glia31990522528
Crossref | PubMed | ISI | Google Scholar
1300 WANG K., WONDERGEM R.Redistribution of hepatocyte chloride during l-alanine uptake.J. Membr. Biol.1351993237244
Crossref | PubMed | ISI | Google Scholar
1301 WANG W., SCHNEIDER E. G.Potassium induced aldosterone secretion involves a Cl dependent mechanism.Am. J. Physiol.272(Regulatory Integrative Comp. Physiol. 41)1997R183R187
Google Scholar
1302 WANG W. J., ACS P., GOODNIGHT J. A., GIESE T., BLUMBERG P. M., MISCHAK H., MUSHINSKI J. F.The catalytic domain of protein kinase C delta in reciprocal delta and epsilon chimeras mediates phorbol ester induced macrophage differentiation of mouse promyelocytes.J. Biol. Chem.27219977682
Crossref | PubMed | ISI | Google Scholar
1303 WANG W.-H., GEIBEL J., GIEBISCH G.Mechanism of apical K⁺ channel modulation in principal renal tubule cells. Effect of inhibition of basolateral Na⁺-K⁺-ATPase.J. Gen. Physiol.1011993673694
Crossref | PubMed | ISI | Google Scholar
1304 WANG, X., C. L., CHIK, A. K. HO, N. SATO, and M. A. GREER. Cyclic adenosine monophosphate is not part of the transduction chain by which cell-swelling induces secretion in either normal or tumor-derived GH₄C₁ pituitary cells. Metabolism 42: 435–439, 1993.
Google Scholar
1305 WANG X., SATO N., GREER M. A.Medium hyperosmolarity inhibits prolactin secretion induced by depolarizing K⁺ in GH₄C₁ cells by blocking Ca²⁺ influx.Mol. Cell. Endocrinol.8319927984
Crossref | PubMed | ISI | Google Scholar
1306 WANG X., SATO N., GREER M. A., GREER S. E., McADAMS S.Cell swelling induced by the permeant molecules urea or glycerol induces immediate high amplitude thyrotropin and prolactin secretion by perifused adenohypophysial cells.Biochem. Biophys. Res. Commun.1631989471475
Crossref | PubMed | ISI | Google Scholar
1307 WANG X., SATO N., GREER M. A., GREER S. E., McADAMS S.Quinidine inhibits prolactin secretion induced by thyrotropin releasing hormone, high medium potassium or hyposmolarity in GH₄C₁ cells.J. Pharmacol. Exp. Ther.2561991135140
PubMed | ISI | Google Scholar
1308 WANG X., SATO N., GREER M. A., GREER S. E., McADAMS S.Role of extracellular calcium and calmodulin in prolactin secretion induced by hyposmolarity, thyrotropin-releasing hormone, and high K⁺ in GH₄C₁ cells.Acta Endocrinol.1231990218224
Crossref | PubMed | Google Scholar
1309 WANG X., SATO N., GREER M. A., McADAMS S., GREER S. E.Dual effect of osmotic cell swelling on prolactin secretion by acutely dispersed adenohypophysial cells.Life Sci.481991617622
Crossref | PubMed | ISI | Google Scholar
1310 WANG Y., ROMAN R., LIDOFSKY S. D., FITZ J. G.Autocrine signaling through ATP release represents a novel mechanism for cell volume regulation.Proc. Natl. Acad. Sci. USA9319961202012025
Crossref | PubMed | ISI | Google Scholar
1311 WANGEMANN P.Comparison of ion transport mechanisms between vestibular dark cells and strial marginal cells.Hearing Res.901995149157
Crossref | PubMed | ISI | Google Scholar
1312 WANGEMANN P., LIU J., SHEN Z., SHIPLEY A., MARCUS D. C.Hypo-osmotic challenge stimulates transepithelial K⁺ secretion and activates apical IsK channel in vestibular dark cells.J. Membr. Biol.1471995263273
Crossref | PubMed | ISI | Google Scholar
1313 WANGEMANN P., LIU J. Z., SHIGA N.Vestibular dark cells contain the Na⁺/H⁺ exchanger NHE 1 in the basolateral membrane.Hearing Res.94199694106
Crossref | PubMed | ISI | Google Scholar
1314 WANGEMANN P., MARCUS D. C.K⁺-induced swelling of vestibular dark cells is dependent on Na⁺ and Cl⁻ and inhibited by piretanide.Pflügers Arch.4161990262269
Crossref | PubMed | ISI | Google Scholar
1315 WANGEMANN P., SHIGA N.Cell volume control in vestibular dark cells during and after a hyposmotic challenge.Am. J. Physiol.266(Cell Physiol. 35)1994C1046C1060
Link | Google Scholar
1316 WARD D. M., PEROU C. M., LLOYD M., KAPLAN J.“Synchronized” endocytosis and intracellular sorting in alveolar macrophages: the early sorting endosome is a transient organelle.J. Cell Biol.129199512291240
Crossref | PubMed | ISI | Google Scholar
1317 WARSKULAT U., NEWSOME W. P., NOE B., STOLL B., HÄUSSINGER D.Anisoosmotic regulation of hepatic gene expression.Biol. Chem. Hoppe-Seyler37719965765
Crossref | PubMed | ISI | Google Scholar
1318 WARSKULAT U., WEIK C., HÄUSSINGER D.Myo-inositol is an osmolyte in rat liver macrophages (Kupffer cells) but not in RAW 264.7 mouse macrophages.Biochem. J.3261997289295
Crossref | PubMed | ISI | Google Scholar
1319 WARSKULAT U., WETTSTEIN M., HÄUSSINGER D.Betaine is an osmolyte in RAW 264.7 mouse macrophages.FEBS Lett.37719954750
Crossref | PubMed | ISI | Google Scholar
1320 WARSKULAT U., WETTSTEIN M., HÄUSSINGER D.Osmoregulated taurine transport in H4IIE hepatoma cells and perfused rat liver.Biochem. J.3211997683690
Crossref | PubMed | ISI | Google Scholar
1321 WARSKULAT U., ZHANG F., HÄUSSINGER D.Modulation of phagocytosis by anisoosmolarity and betaine in rat liver macrophages (Kupffer cells) and raw 264.7 mouse macrophages.FEBS Lett.3911996287292
Crossref | PubMed | ISI | Google Scholar
1322 WARSKULAT U., ZHANG F., HÄUSSINGER D.Taurine is an osmolyte in rat liver macrophages (Kupffer cells).J. Hepatol.26199713401347
Crossref | PubMed | ISI | Google Scholar
1323 WASSERMAN J. C., DELPIRE E., TONIDANDEL W., KOJIMA R., GULLANS S. R.Molecular characterization of ROSIT, a renal osmotic stress-induced Na⁺-Cl⁻-organic solute cotransporter.Am. J. Physiol.267(Renal Fluid Electrolyte Physiol. 36)1994F688F694
Google Scholar
1324 WATSON P. A.Accumulation of cAMP and calcium in S49 mouse lymphoma cells following hyposmotic swelling.J. Biol. Chem.26419891473514740
PubMed | ISI | Google Scholar
1325 WATSON P. A.Direct stimulation of adenylate cyclase by mechanical forces in S49 mouse lymphoma cells during hyposmotic swelling.J. Biol. Chem.265199065696575
PubMed | ISI | Google Scholar
1326 WATSON P. A.Function follows form: generation of intracellular signals by cell deformation.FASEB J.5199120132019
Crossref | PubMed | ISI | Google Scholar
1327 WEBER K., OSBORN M.The cytoskeleton.Natl. Cancer Inst. Monogr.6019823146
PubMed | Google Scholar
1328 WEEL J. F. L., VAN PUTTEN J. P.Fate of the major outer membrane protein P.IA in early and late events of gonococcal infection of epithelial cells.Res. Microbiol.1421991985993
Crossref | PubMed | ISI | Google Scholar
1329 WEHLING, M., J. KASMAYR, and K. THEISEN. Rapid effects of mineralcorticoids on sodium-proton exchanger: genomic or nongenomic pathway? Am. J. Physiol. 260 (Endocrinol. Metab. 23): E719–E726, 1991.
Google Scholar
1330 WEHLING M., KASMAYR J., THEISEN K.The Na⁺-H⁺ exchanger is stimulated and cell volume increased in lymphocytes from patients with essential hypertension.J. Hypertens.91991519524
Crossref | PubMed | ISI | Google Scholar
1331 WEHLING M., KUHLS S., ARMANINI D.Volume regulation of human lymphocytes by aldosterone in isotonic media.Am. J. Physiol.257(Endocrinol. Metab. 20)1989E170E174
Google Scholar
1332 WEHNER F., SAUER H., KINNE R. K. H.Hypertonic stress increases the Na⁺ conductance of rat hepatocytes in primary culture.J. Gen. Physiol.1051995507535
Crossref | PubMed | ISI | Google Scholar
1333 WEI L.-Y., ROEPE P. D.Low external pH and osmotic shock increase the expression of human MDR protein.Biochemistry33199472297238
Crossref | PubMed | ISI | Google Scholar
1334 WEISS H., LANG F.Ion channels activated by swelling of Madin-Darby canine kidney (MDCK) cells.J. Membr. Biol.1261992109114
Crossref | PubMed | ISI | Google Scholar
1335 WEISSBACH L., KILBERG M. S.Amino acid activation of amino acid transport system N early in primary cultures of rat hepatocytes.J. Cell. Physiol.1211984133138
Crossref | PubMed | ISI | Google Scholar
1336 WELSH M. J.Electrolyte transport by airway epithelia.Physiol. Rev.67198711431184
Link | ISI | Google Scholar
1337 WELSH M. J., LIEDTKE C. M.Chloride and potassium channels in cystic fibrosis airway epithelia.Nature3221986467470
Crossref | PubMed | ISI | Google Scholar
1338 WELTE W.Porins from bacterial outer membranes.Renal Physiol. Biochem.171994216218
PubMed | Google Scholar
1339 WESTBROOK G. L.Glutamate receptors and excitotoxicity.Res. Publ. Assoc. Res. Nerv. Ment. Dis.7119933550
PubMed | Google Scholar
1340 WETTSTEIN M., NOE B., HÄUSSINGER D.Metabolism of cysteinyl leukotrienes in the perfused rat liver: the influence of endotoxin pretreatment and the cellular hydration state.Hepatology221995235240
PubMed | ISI | Google Scholar
1341 WETTSTEIN M., VOM S.DAHL, F. LANG, W. GEROK, and D. HÄUSSINGER. Cell volume regulatory responses of isolated perfused rat liver. The effect of amino acids.Biol. Chem. Hoppe-Seyler3711990493501
Crossref | PubMed | ISI | Google Scholar
1342 WHALLEY D. W., HOOL L. C., TEN EICK R. E., RASMUSSEN H. H.Effect of osmotic swelling and shrinkage on Na⁺-K⁺ pump activity in mammalian cardiac myocytes.Am. J. Physiol.265(Cell Physiol. 34)1993C1201C1210
Link | Google Scholar
1343 WHEATLEY D. N.Cell growth and division in hypertonic medium.Exp. Cell Res.871974219232
Crossref | PubMed | ISI | Google Scholar
1344 WIEBEL F. J., KLOSE U., KIEFER F.Toxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin in vitro: H4IIEC3-derived 5L hepatoma cells as a model system.Toxicol. Lett.551991161169
Crossref | PubMed | ISI | Google Scholar
1345 WIESINGER H., THEISS U., HAMPRECHT B.Sorbitol pathway activity and utilization of polyols in astroglia-rich primary cultures.Glia31990277282
Crossref | PubMed | ISI | Google Scholar
1346 WILKER C. E., WELSH T. H.Jr., S. H. SAFE, T. R. NARASIMHAN, and L. JOHNSON. Human chorionic gonadotropin protects Leydig cell function against 2,3,7,8-tetrachloridibenzo-p-dioxin in adult rats: role of Leydig cells cytoplasmic volume.Toxicology95199593102
Crossref | PubMed | ISI | Google Scholar
1347 WILLS N. K., MILLINOFF L. P., CROWE W. E.Na⁺ channel activity in cultured renal (A6) epithelium: regulation by solution osmolarity.J. Membr. Biol.12119917990
Crossref | PubMed | ISI | Google Scholar
1348 WILLUMSEN N. J., DAVIS C. W., BOUCHER R. C.Selective response of human airway epithelia to luminal but not serosal solution hypertonicity. Possible role for proximal airway epithelia as an osmolality transducer.J. Clin. Invest.941994779787
Crossref | PubMed | ISI | Google Scholar
1349 WINDHAGER E. E., TAYLOR A.Regulatory role of intracellular calcium ions in epithelial Na transport.Annu. Rev. Physiol.451983519532
Crossref | PubMed | ISI | Google Scholar
1350 WINTER M., CARSON M., SHASBY M.Mastoparan activates apical chloride and potassium conductances, decreases cell volume, and increases permeability of cultured epithelial cell monolayers.Am. J. Respir. Cell Mol. Biol.61992583593
Crossref | PubMed | ISI | Google Scholar
1351 WINZOR C. L., WINZOR D. J., PALEG L. G., JONES G. P., NAIDU B. P.Rationalization of the effects of compatible solutes on protein stability in terms of thermodynamic nonideality.Arch. Biochem. Biophys.2961992102107
Crossref | PubMed | ISI | Google Scholar
1352 WIRTHENSOHN, G., S. LE FRANK, and W. G. GUDER. Studies on the role of glycerophosphorylcholine and sorbitol in renal osmoregulation. In: Molecular Nephrology. Biochemical Aspects of Kidney Function, edited by Z. Kovacevic and W. G. Guder. Berlin: de Gruyter, 1987, p. 321–327.
Google Scholar
1353 WIRTHENSOHN G., LEFRANK S., SCHMOLKE M., GUDER W. G.Regulation of organic osmolyte concentrations in tubules from rat renal inner medulla.Am. J. Physiol.256(Renal Fluid Electrolyte Physiol. 25)1989F128F135
Google Scholar
1354 WIRTZ H. R. W., DOBBS L. G.Calcium mobilization and exocytosis after one mechanical stretch of lung epithelial cells.Science250199012661269
Crossref | PubMed | ISI | Google Scholar
1355 WITKE W., SHARPE A. H., HARTWIG J. H., AZUMA T., STOSSEL T. P., KWIATKOWSKI D. J.Hemostatic, inflammatory, and fibroblast responses are blunted in mice lacking gelsolin.Cell8119954151
Crossref | PubMed | ISI | Google Scholar
1356 WOLFF S. D., STANTON T. S., JAMES S. L., BALABAN R. S.Acute regulation of the predominant organic solutes of the rabbit renal inner medulla.Am. J. Physiol.257(Renal Fluid Electrolyte Physiol. 26)1989F676F681
Google Scholar
1357 WÖLL E., RITTER M., HALLER T., VÖLKL H., LANG F.Calcium entry stimulated by swelling of Madin-Darby canine kidney (MDCK) cells.Nephron741996150157
Crossref | PubMed | ISI | Google Scholar
1358 WÖLL E., RITTER M., SCHOLZ W., HÄUSSINGER D., LANG F.The role of calcium in cell shrinkage and intracellular alkalinization by bradykinin in Ha-ras oncogene expressing cells.FEBS Lett.3221993261265
Crossref | PubMed | ISI | Google Scholar
1359 WÖLL E., WALDEGGER S., LANG F., MALY K., GRUNICKE H.Mechanism of intracellular calcium oscillations in fibroblasts expressing the ras oncogene.Pflügers Arch.4201992208212
Crossref | PubMed | ISI | Google Scholar
1360 WÖLL E., WEISS H., WALDEGGER S., LANG F.Effect of calcium channel antagonists on cell membrane potential oscillations and proliferation of cells expressing the ras oncogene.Eur. J. Pharmacol.2121992105107
Crossref | PubMed | ISI | Google Scholar
1361 WOLLNIK B., KUBISCH C., MAASS A., VETTER H., NEYSES L.Hyperosmotic stress induces immediate-early gene expression in ventricular adult cardiomyocytes.Biochem. Biophys. Res. Commun.1941993642646
Crossref | PubMed | ISI | Google Scholar
1362 WONDERGEM R., DAVIS J.Ethanol increases hepatocyte water volume.Alcohol. Clin. Exp. Res.18199412301236
Crossref | PubMed | ISI | Google Scholar
1363 WONG M. M., FOSKETT J. K.Oscillations of cytosolic sodium during calcium oscillations in exocrine acinar cells.Science254199110141016
Crossref | PubMed | ISI | Google Scholar
1364 WORRELL R. T., BUTT A. G., CLIFF W. H., FRIZZELL R. A.A volume-sensitive chloride conductance in human colonic cell line T84.Am. J. Physiol.256(Cell Physiol. 25)1989C1111C1119
Link | Google Scholar
1365 WORTHEN G. S., HENSON P. M., ROSENGREN S., DOWNEY G. P., HYDE D. M.Neutrophils increase volume during migration in vivo and in vitro.Am. J. Respir. Cell Mol. Biol.10199417
Crossref | PubMed | ISI | Google Scholar
1366 WU G., FLYNN N. E.Regulation of glutamine and glucose metabolism by cell volume in lymphocytes and macrophages.Biochim. Biophys. Acta12431995343350
Crossref | PubMed | ISI | Google Scholar
1367 WYLLIE A. H., KERR J. F., CURRIE A. R.Cell death: the significance of apoptosis.Int. Rev. Cytol.681980251306
Crossref | PubMed | Google Scholar
1368 XIA Z., DICKENS M., RAINGEAUD J., DAVIS R. J., GREENBERG M. E.Opposing effects of ERK and JNK-p38 MAP kinases on apoptosis.Science270199513261331
Crossref | PubMed | ISI | Google Scholar
1369 XU B., WILSON B. A., LU L.Induction of human myeloblastic ML 1 cell G₁ arrest by suppression of K⁺ channel activity.Am. J. Physiol.271(Cell Physiol. 40)1996C2037C2044
Link | Google Scholar
1370 XU J.-C., LYTLE C., ZHU T. T., PAYNE J. A., BENZ E.Jr., and B. FORBUSH III. Molecular cloning and functional expression of the bumetanide-sensitive Na-K-Cl cotransporter.Proc. Natl. Acad. Sci. USA91199422012205
Crossref | PubMed | ISI | Google Scholar
1371 YAMAMOTO T., MUNDY C. A., WILSON C. B., BLANTZ R. C.Effect of mesangial cell lysis and proliferation on glomerular hemodynamics in the rat.Kidney Int.401991705713
Crossref | PubMed | ISI | Google Scholar
1372 YAMAUCHI A., KWON H. M., UCHIDA S., PRESTON A. S., HANDLER J. S.Myo-inositol and betaine transporters regulated by tonicity are basolateral in MDCK cells.Am. J. Physiol.261(Renal Fluid Electrolyte Physiol. 30)1991F197F202
Google Scholar
1373 YAMAUCHI A., MIYAI A., YOKOYAMA K., ITOH T., KAMADA T., UEDA N., FUJIWARA Y.Response to osmotic stimuli in mesangial cells: role of system A transporter.Am. J. Physiol.267(Cell Physiol. 36)1994C1493C1500
Link | Google Scholar
1374 YAMAUCHI A., UCHIDA S., KWON H. M., PRESTON A. S., ROBEY R. B., GARCIA-PEREZ A., BURG M. B., HANDLER J. S.Cloning of a Na⁺- and Cl⁻-dependent betaine transporter that is regulated by hypertonicity.J. Biol. Chem.2671992649652
PubMed | ISI | Google Scholar
1375 YAMAUCHI A., SUGIURA T., ITO T., MIYAI A., HORIO M., IMAI E., KAMADA T.Na⁺/myo-inositol transport is regulated by basolateral tonicity in Madin-Darby canine kidney cells.J. Clin. Invest.971996263267
Crossref | PubMed | ISI | Google Scholar
1376 YANCEY, P. H. Compatible and conteracting solutes. In: Cellular and Molecular Physiology of Cell Volume Regulation, edited by K. Strange. Boca Raton, FL: CRC, 1994, p. 81–109.
Google Scholar
1377 YANCEY P. H.Osmotic effectors in kidneys of xeric and mesic rodents: corticomedullary distributions and changes with water availability.J. Comp. Physiol. B Biochem. Syst. Environ. Physiol.1581988369380
Crossref | PubMed | ISI | Google Scholar
1378 YANCEY P. H., BURG M. B.Distribution of major organic osmolytes in rabbit kidneys in diuresis and antidiuresis.Am. J. Physiol.257(Renal Fluid Electrolyte Physiol. 26)1989F602F607
Google Scholar
1379 YANCEY P. H., BURG M. B., BAGNASCO S. M.Effects of NaCl, glucose and aldose reductase inhibitors on cloning efficiency of renal medullary cells.Am. J. Physiol.258(Cell Physiol. 27)1990C156C163
Link | Google Scholar
1380 YANCEY P. H., BURG M. B.Counteracting effects of urea and betaine in mammalian cells in culture.Am. J. Physiol.258(Regulatory Integrative Comp. Physiol. 27)1990R198R204
Google Scholar
1381 YANCEY P. H., CLARK M. E., HAND S. C., BOWLUS R. D., SOMERO G. N.Living with water stress: evolution of osmolyte systems.Science217198212141222
Crossref | PubMed | ISI | Google Scholar
1382 YANCEY P. H., SOMERO G. N.Counteraction of urea destabilization of protein structure by methylamine osmoregulatory compounds of elasmobranch fishes.Biochem. J.1831979317323
Crossref | PubMed | ISI | Google Scholar
1383 YANCEY P. H., SOMERO G. N.Methylamine osmoregulatory solutes of elasmobranch fishes counteract urea inhibition of enzymes.J. Exp. Zool.2121980205213
Crossref | Google Scholar
1384 YANKASKAS J. R., GATZY J. T., BOUCHER R. C.Effects of raised osmolarity on canine tracheal epithelial ion transport function.J. Appl. Physiol.62198722412245
Link | ISI | Google Scholar
1385 YANTORNO R. E., CARRE D. A., COCA M.PRADOS, T. KRUPIN, and M. M. CIVAN. Whole cell patch clamping of ciliary epithelial cells during anisosmotic swelling.Am. J. Physiol.262(Cell Physiol. 31)1992C501C509
Link | Google Scholar
1386 YOREK M. A., DUNLAP J. A., GINSBERG B. H.Effect of increased glucose levels on Na⁺/K⁺ pump activity in cultured neuroblastoma cells.J. Neurochem.511988601610
ISI | Google Scholar
1387 YOREK M. A., DUNLAP J. A., STEFANI M. R.Restoration of Na⁺/K⁺ pump activity and resting membrane potential by myo-inositol supplementation in neuroblastoma cells chronically exposed to glucose or galactose.Diabetes401991240248
Crossref | PubMed | ISI | Google Scholar
1388 YOUNG E., BRADLEY R. F.Cerebral edema with irreversible coma in severe diabetic ketoacidosis.N. Engl. J. Med.2761967665669
Crossref | PubMed | ISI | Google Scholar
1389 ZAMMIT V. A.Effect of hydration state on the synthesis and secretion of triacylglycerol by isolated rat hepatocytes. Implications for the actions of insulin and glucagon on hepatic secretion.Biochem. J.31219955762
Crossref | PubMed | ISI | Google Scholar
1390 ZENTAY Z., REDDI A., RAGUWANSHI M., GARDNER J. P., CHO J. H., LASKER N., DASMAHAPATRA A., AVIV A.Platelet sodium-hydrogen antiport in obese and diabetic black women.Hypertension201992549554
Crossref | PubMed | ISI | Google Scholar
1391 ZHANG F., WETTSTEIN M., WARSKULAT U., SCHREIBER R., HENNINGER P., DECKER K., HÄUSSINGER D.Hyperosmolarity stimulates prostaglandin synthesis and cyclooxygenase-2 expression in activated rat liver macrophages.Biochem. J.3121995135143
Crossref | PubMed | ISI | Google Scholar
1392 ZHANG F., WARSKULAT U., HÄUSSINGER D.Modulation of tumor necrosis factor alpha release by anisoosmolarity and betaine in rat liver macrophages (Kupffer cells).FEBS Lett.3911996293296
Crossref | PubMed | ISI | Google Scholar
1393 ZHANG F., WARSKULAT U., WETTSTEIN M., HÄUSSINGER D.Identification of betaine as an osmolyte in rat liver macrophages (Kupffer cells).Gastroenterology110199615431552
Crossref | PubMed | ISI | Google Scholar
1394 ZHANG J., RASMUSSON R. L., HALL S. K., LIEBERMAN M.A chloride current associated with swelling of cultured chick heart cells.J. Physiol. (Lond.)4721993801820
Crossref | Google Scholar
1395 ZHAO Y., CHIEN S., SKALAK R.A stochastic model of leukocyte rolling.Biophys. J.69199513091320
Crossref | PubMed | ISI | Google Scholar
1396 ZIMMER M., KEMPSKI O., NEU A., VON ROSEN F., BAETHMANN A.Anoxic incubation of suspended glial cells. An in-vitro model of cerebral anoxia to study cytotoxic brain edema.Adv. Neurosurg.121984271273
Crossref | Google Scholar
1397 ZIMMERMAN S. B., MINTON A. P.Macromolecular crowding: biochemical, biophysical, and physiological consequences.Annu. Rev. Biophys. Biomol. Struct.2219932765
Crossref | PubMed | Google Scholar
1398 ZIYADEH F. N., MILLS J. W., KLEINZELLER A.Hypotonicity and cell volume regulation in shark rectal gland: role of organic osmolytes and F-actin.Am. J. Physiol.262(Renal Fluid Electrolyte Physiol. 31)1992F468F479
Google Scholar
1399 ZONGAZO M. A., CARAYON A., MASSON F., ISNARD R., EURIN J., MAISTRE G., BARTHELEMY C., PROST A. C., LEGRAND J. C.Atrial natriuretic peptide during water deprivation or hemorrhage in rats. Relationship with arginine vasopressin and osmolarity.J. Physiol. (Paris)861992167175
Crossref | PubMed | Google Scholar
1400 ZONGAZO M. A., CARAYON A., MASSON F., MAISTRE G., NOE E., EURIN J., BARTHELEMY C., KOMAJDA M., LEGRAND J. C.Effects of arginine vasopressin and extracellular osmolarity on atrial natriuretic peptide release by superfused rat atria.Eur. J. Pharmacol.20919914555
Crossref | PubMed | ISI | Google Scholar

Volume 78Issue 1January 1998Pages 247-306

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Published online 1 January 1998

Published in print 1 January 1998

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Functional Significance of Cell Volume Regulatory Mechanisms

Abstract

I. INTRODUCTION

II. CELL VOLUME REGULATORY MECHANISMS

A. Ions in Steady-State Maintenance of Cell Volume

B. Volume Regulatory Ion Transport

1. Regulatory cell volume decrease

2. Regulatory cell volume increase

C. Osmolytes

1. Glycerophosphorylcholine

2. Sorbitol

3. Inositol

4. Betaine

5. Taurine

6. Amino acids

D. Further Metabolic Pathways Contributing to Cell Volume Regulation

III. INTRACELLULAR SIGNALING OF CELL VOLUME REGULATION

A. Macromolecular Crowding

B. Cytoskeleton

1. Actin filaments

2. Microtubules

C. Cell Membrane Stretch

D. Cell Membrane Potential

E. Cytosolic pH

F. Calcium

G. G Proteins

H. Protein Phosphorylation

1. Cell swelling

2. Cell shrinkage

I. Chloride

J. Magnesium

K. Eicosanoids

L. pH in Acidic Cellular Compartments

M. Gene Expression

IV. CHALLENGES OF CELL VOLUME CONSTANCY

A. Alterations of Extracellular Osmolarity

B. Alterations of Extracellular Ion Composition

C. Energy Depletion

D. Ion Transport Altered by Hormones and Transmitters

E. Substrate Transport

F. Metabolism

G. Others

V. ROLE OF CELL VOLUME REGULATORY MECHANISMS IN CELL FUNCTIONS

A. Erythrocyte Function

B. Epithelial Transport

C. Regulation of Metabolism

D. Receptor Recycling

E. Hormone and Transmitter Release

F. Excitability and Contraction

G. Migration

H. Pathogen Host Interactions

I. Cell Proliferation

J. Cell Death

K. Others

REFERENCES

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