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Am J Physiol Gastrointest Liver Physiol 281: G1369-G1377, 2001;
0193-1857/01 $5.00
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Vol. 281, Issue 6, G1369-G1377, December 2001

Colonic H+-K+-ATPase in K+ conservation and electrogenic Na+ absorption during Na+ restriction

Zachary Spicer1, Lane L. Clarke2, Lara R. Gawenis2, and Gary E. Shull1

1 Department of Molecular Genetics, Biochemistry and Microbiology, The University of Cincinnati College of Medicine, Cincinnati, Ohio 45267-0524; and 2 Department of Biomedical Sciences, College of Veterinary Medicine and Dalton Cardiovascular Research Center, University of Missouri, Columbia, Missouri 65211

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.

Atp1al1; potassium absorption; sodium absorption; hydrogen secretion


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