Isolated trout hepatocytes exposed to hypotonic Hank's medium (isotonicity × 0.70) swelled to 1.17 times the control volume after 3 min; by 15 min the cell volume had returned to normal. The ouabain-insensitive K+ uptake increased, indicating an immediate rise in K+ membrane permeability. As indicated by analysis of cellular contents, the regulatory volume decrease (RVD) was ensured by a release of intracellular K+. Na+ was not implicated in this mechanism. This potassium permeability induced by hypotonic shock was transient (maximum at 6 min), insensitive to blocking agents of voltage- and Ca2+-dependent K+ channels, and chloride-dependent. This result, together with a time-course of Cl- uptake similar to that of K+, suggests a K+/Cl- cotransport mechanism. This cotransport is inhibited by high furosemide concentrations (10(−3) mol l-1) but not by bumetanide (10(−4) mol l-1) or piretanide (10(−4) mol l-1).
Effects of hyposmotic shock on ion fluxes in isolated trout hepatocytes
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L. Bianchini, B. Fossat, J. Porthe-Nibelle, J. C. Ellory, B. Lahlou; Effects of hyposmotic shock on ion fluxes in isolated trout hepatocytes. J Exp Biol 1 July 1988; 137 (1): 303–318. doi: https://doi.org/10.1242/jeb.137.1.303
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