Potassium permeability and volume control in isolated rat hepatocytes

Bakker-Grunwald, Tilly

doi:10.1016/0005-2736(83)90014-7

Cited by 92 publications

(24 citation statements)

References 7 publications

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“…Cell shrinkage was achieved by inhibition of the major ion uptake mechanisms Na ϩ ͞H ϩ exchanger (28-30) and the NaCl͞KCl cotransporter (31, 32) by their specific blockers HOE694 and bumetanide, respectively. Cell swelling induced by the addition of amino acids is due to the concentrative uptake of amino acids by means of Na ϩ -dependent amino acid transporters such as system A, N, and ASC in the plasma membrane of hepatocytes (33)(34)(35)(36)(37)(38)(39)(40). Thus, the transcript levels were correlated with cell volume rather than osmolarity.…”

Section: Discussionmentioning

confidence: 87%

Cloning and characterization of a putative human serine/threonine protein kinase transcriptionally modified during anisotonic and isotonic alterations of cell volume

Waldegger

Barth²,

Raber³

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

336

328

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Hepatic metabolism and gene expression are among other regulatory mechanisms controlled by the cellular hydration state, which changes rapidly in response to anisotonicity, concentrative substrate uptake, oxidative stress, and under the inf luence of hormones such as insulin and glucagon. Differential screening for cell volume sensitive transcripts in a human hepatoma cell line revealed a gene for a putative serine͞threonine kinase, h-sgk, which has 98% sequence identity to a serum-and glucocorticoid regulated kinase, sgk, cloned from a rat mammary tumor cell line. h-sgk transcript levels were strongly altered during anisotonic and isotonic cell volume changes. Within 30 min h-sgk RNA was, independent of de novo protein synthesis, induced upon cell shrinkage and, due to a complete stop in h-sgk transcription, reduced upon cell swelling. Comparable changes of sgk transcript levels were observed in a renal epithelial cell line. h-sgk mRNA was detected in all human tissues tested, with the highest levels in pancreas, liver, and heart. The putative serine͞threonine protein kinase h-sgk may provide a functional link between the cellular hydration state and metabolic control.

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Section: Discussionmentioning

confidence: 87%

Cloning and characterization of a putative human serine/threonine protein kinase transcriptionally modified during anisotonic and isotonic alterations of cell volume

Waldegger

Barth²,

Raber³

et al. 1997

Proc. Natl. Acad. Sci. U.S.A.

336

328

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“…1). In hepatocytes, as well as other cells of most vertebrates, swelling triggers a volume regulatory response that is largely mediated by an increased plasma membrane conductance for K + and Cl - (Bakker-Grunwald, 1983;Wehner et al, 1992;Wang et al, 1996;Roe et al, 2001). However, unlike hepatocytes of trout and rat, experiments using videomicroscopy (Figs 1, 2) and fluorescence microscopy (not shown) showed that goldfish hepatocytes displayed no (pH 7.45) or only a slight (pH 7.8) RVD.…”

Section: Discussionmentioning

confidence: 98%

Volumetric and ionic responses of goldfish hepatocytes to anisotonic exposure and energetic limitation

Espelt

Mut

Amodeo

et al. 2003

Journal of Experimental Biology

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SUMMARYThe relationship between cell volume and K+ transmembrane fluxes of goldfish (Carassius auratus) hepatocytes exposed to anisotonic conditions or energetic limitation was studied and compared with the response of hepatocytes from trout (Oncorhynchus mykiss) and rat (Rattus rattus). Cell volume was studied by video- and fluorescence microscopy,while K+ fluxes were assessed by measuring unidirectional 86Rb+ fluxes.In trout and rat hepatocytes, hyposmotic (180 mosmoll-1)exposure at pH 7.45 caused cell swelling followed by a regulatory volume decrease (RVD), a response reported to be mediated by net efflux of KCl and osmotically obliged water. By contrast, goldfish hepatocytes swelled but showed no RVD under these conditions. Although in goldfish hepatocytes a net(86Rb+)K+ efflux could be activated by N-ethylmaleimide, this flux was not, or only partially, activated by hyposmotic swelling (120-180 mosmoll-1).Blockage of glycolysis by iodoacetic acid (IAA) did not alter cell volume in goldfish hepatocytes, whereas in the presence of cyanide (CN-),an inhibitor of oxidative phosphorylation, or CN- plus IAA(CN-+IAA), cell volume decreased by 3-7%. Although in goldfish hepatocytes, energetic limitation had no effect on(86Rb+)K+ efflux,(86Rb+)K+ influx decreased by 57-66% in the presence of CN- and CN-+IAA but was not significantly altered by IAA alone. Intracellular K+ loss after 20 min of exposure to CN- and CN-+IAA amounted to only 3% of the total intracellular K+.Collectively, these observations suggest that goldfish hepatocytes, unlike hepatocytes of anoxia-intolerant species, avoid a decoupling of transmembrane K+ fluxes in response to an osmotic challenge. This may underlie both the inability of swollen cells to undergo RVD but also the capability of anoxic cells to maintain intracellular K+ concentrations that are almost unaltered, thereby prolonging cell survival.

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“…Cell volume regulation may also be mediated via loop-diuretic insensitive pathways; exposure of cells to hypotonic media often results in a specific increase in passive membrane K § permeability which is associated with a net loss of intracellular KC1 and subsequent cell shrinkage (volume-regulatory decrease) [5,9,10,24,35,41]. Since membrane K § conductance may be limited by anion permeability, separate conductive ion channels for both K + and Cl-may be stimulated by cellular swelling [18,20].…”

Section: Introductionmentioning

confidence: 99%

Role of passive potassium fluxes in cell volume regulation in cultured HeLa cells

1985

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Cultured HeLa cells behave as ideal osmometers when subjected to hyperosmolar media, and show no volume regulatory behavior. In hypoosmolar solutions, cell swelling is not as great as predicted, and this is due largely to a loss of intracellular KCl. In hyperosmolar solutions there is a stimulation of the ouabain-insensitive but loop diuretic-sensitive 86Rb+ (K+) pathway. Analysis of the K+, Na+ and Cl- dependency of this K+ flux pathway demonstrates that the increase is principally due to an increase in its maximal velocity (Vmax). The sensitivity of this pathway to diuretic inhibition is unchanged in hyperosmolar media. Diuretic-sensitive 86Rb+ (K+) efflux stimulated by hypertonicity shows no marked dependence on external K+. The K+ loss observed in hypoosmolar media is distinct from the K+ transport pathway stimulated by hyperosmolar media on the basis of its sensitivity to furosemide and anion dependence.

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Potassium permeability and volume control in isolated rat hepatocytes

Cited by 92 publications

References 7 publications

Cloning and characterization of a putative human serine/threonine protein kinase transcriptionally modified during anisotonic and isotonic alterations of cell volume

Cloning and characterization of a putative human serine/threonine protein kinase transcriptionally modified during anisotonic and isotonic alterations of cell volume

Volumetric and ionic responses of goldfish hepatocytes to anisotonic exposure and energetic limitation

Role of passive potassium fluxes in cell volume regulation in cultured HeLa cells

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