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Publication : Colonic H(+)-K(+)-ATPase in K(+) conservation and electrogenic Na(+) absorption during Na(+) restriction.

First Author  Spicer Z Year  2001
Journal  Am J Physiol Gastrointest Liver Physiol Volume  281
Issue  6 Pages  G1369-77
PubMed ID  11705741 Mgi Jnum  J:108059
Mgi Id  MGI:3622951 Doi  10.1152/ajpgi.2001.281.6.G1369
Citation  Spicer Z, et al. (2001) Colonic H(+)-K(+)-ATPase in K(+) conservation and electrogenic Na(+) absorption during Na(+) restriction. Am J Physiol Gastrointest Liver Physiol 281(6):G1369-77
abstractText  Upregulation of the colonic H(+)-K(+)- ATPase (cHKA) during hyperaldosteronism suggests that it functions in both K(+) conservation and electrogenic Na(+) absorption in the colon when Na(+)-conserving mechanisms are activated. To test this hypothesis, wild-type (cHKA(+/+)) and cHKA-deficient (cHKA(-/-)) mice were fed Na(+)-replete and Na(+)-restricted diets and their responses were analyzed. In both genotypes, Na(+) restriction led to reduced plasma Na(+) and increased serum aldosterone, and mRNAs for the epithelial Na(+) channel (ENaC) beta- and gamma-subunits, channel-inducing factor, and cHKA were increased in distal colon. Relative to wild-type controls, cHKA(-/-) mice on a Na(+)-replete diet had elevated fecal K(+) excretion. Dietary Na(+) restriction led to increased K(+) excretion in knockout but not in wild-type mice. The amiloride-sensitive, ENaC-mediated short-circuit current in distal colon was significantly reduced in knockout mice maintained on either the Na(+)-replete or Na(+)-restricted diet. These results demonstrate that cHKA plays an important role in K(+) conservation during dietary Na(+) restriction and suggest that cHKA-mediated K(+) recycling across the apical membrane is required for maximum electrogenic Na(+) absorption.
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