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Effect of hypertonic stress on liver cell volume bile flow and volume regulatory potassium fluxes

Effect of hypertonic stress on liver cell volume bile flow and volume regulatory potassium fluxes

American Journal of Physiology 256(3 Part 1): G563-G569

ISSN/ISBN: 0363-6143

Net hepatic uptake and release of K+ were studied in the isolated-perfused rat liver subjected to a 10-min period of hyperosmotic stress by addition of 80 mM mannitol or sucrose to the perfusing solution. Bile flow and effluent Na+, K+, and Ca2+ activities were monitored throughout. Upon initiation of hypertonic stress, a sharp transient dilution of effluent ion activities indicated hepatic water losses that were larger and occurred more rapidly with sucrose than with mannitol. During continuous hyperosmotic perfusion, portocaval differences in K+ uncovered a steady net influx of the ion into the liver that reached a higher maximum and led to a greater accumulation in experiments with sucrose compared with mannitol. This hepatic K+ uptake was completely blocked by 1 mM ouabain. Upon return to isotonic conditions, a sharp transient concentration of effluent ion activities suggested hepatic water uptake that was again more rapid and pronounced in sucrose- than mannitol-treated livers. This was followed by a transient phase of net hepatic K+ release whose magnitude and duration were proportional to the water movements induced by the removal of each carbohydrate. Administration of 2 mM Ba2+ abolished this K+ efflux. These results indicate that mannitol equilibrates between extra- and intracellular compartments, whereas sucrose apparently does not. The data also suggest that net movements of K+ may be involved in the regulatory volume responses induced by hyperosmotic stress and return to normal tonicity, respectively.

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Accession: 007250060

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