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Intracellular alkalinization stimulates bile flow and vesicular-mediated exocytosis in IPRL

Intracellular alkalinization stimulates bile flow and vesicular-mediated exocytosis in IPRL CHLORIDE-BICARBONATE EXCHANGE mechanisms regulate intracellular pH (pHi) by functioning as acid loaders in various mammalian (8, 20) and nonmammalian cells (26). The presence of a Cl--HCO; exchanger in hepatocytes was first identified in canalicular plasma membrane vesicles from rat liver (21) and was subsequently confirmed in hepatoma cells (28) and in isolated rat hepatocytes (4). The latter studies demonstrated that the Cl--HCO; exchanger mediates recovery of pHi from an alkaline load and is electroneutral, Na+ independent, and sensitive to the anion exchanger inhibitor 4,4’-diisothiocyanostilbene-2,2’-disulfonic acid (DIDS) (4). These studies also demonstrated that the activity of the apical Cl--HCO; exchanger was directly proportional to pHi, raising the possibility that intracellular alkalosis might represent a signal for biliary HCO, secretion. Clearly, if these observations in isolated rat hepatocytes have functional significance, acute intracellular should enhance biliary HCO; secretion and possibly bile flow (2, 16, 27) in the intact liver. More recent studies, again in isolated rat hepatocytes, have observed that cells incubated for 2-6 h in HCO;-containing media showed for any given intracellular HCO; concentration 0193-1857/93 $2.00 Copyright ([HCO;]), a higher Cl--HCO, exchange activity compared with cells cultured in the nominal absence of HCO;. These findings suggest that the number http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png AJP - Gastrointestinal and Liver Physiology The American Physiological Society

Intracellular alkalinization stimulates bile flow and vesicular-mediated exocytosis in IPRL

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Publisher
The American Physiological Society
Copyright
Copyright © 1993 the American Physiological Society
ISSN
0193-1857
eISSN
1522-1547
Publisher site
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Abstract

CHLORIDE-BICARBONATE EXCHANGE mechanisms regulate intracellular pH (pHi) by functioning as acid loaders in various mammalian (8, 20) and nonmammalian cells (26). The presence of a Cl--HCO; exchanger in hepatocytes was first identified in canalicular plasma membrane vesicles from rat liver (21) and was subsequently confirmed in hepatoma cells (28) and in isolated rat hepatocytes (4). The latter studies demonstrated that the Cl--HCO; exchanger mediates recovery of pHi from an alkaline load and is electroneutral, Na+ independent, and sensitive to the anion exchanger inhibitor 4,4’-diisothiocyanostilbene-2,2’-disulfonic acid (DIDS) (4). These studies also demonstrated that the activity of the apical Cl--HCO; exchanger was directly proportional to pHi, raising the possibility that intracellular alkalosis might represent a signal for biliary HCO, secretion. Clearly, if these observations in isolated rat hepatocytes have functional significance, acute intracellular should enhance biliary HCO; secretion and possibly bile flow (2, 16, 27) in the intact liver. More recent studies, again in isolated rat hepatocytes, have observed that cells incubated for 2-6 h in HCO;-containing media showed for any given intracellular HCO; concentration 0193-1857/93 $2.00 Copyright ([HCO;]), a higher Cl--HCO, exchange activity compared with cells cultured in the nominal absence of HCO;. These findings suggest that the number

Journal

AJP - Gastrointestinal and Liver Physiology – The American Physiological Society

Published: Aug 1, 1993

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