11457729

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2

Apical H-K-ATPase in the cortical collecting duct (CCD) plays an important role in urinary acidification and K reabsorption. Our previous studies demonstrated that an H-K-ATPase mediates, in part, Rb reabsorption in rabbit CCD (Zhou X and Wingo CS. Am J Physiol Renal Fluid Electrolyte Physiol 263: F1134-F1141, 1992). The purpose of these experiments was to examine using in vitro microperfused CCD from K-restricted rabbits 1) whether an acute increase in PCO(2) and, presumably, intracellular acidosis stimulate K absorptive flux; and 2) whether this stimulation was dependent on the presence of a functional H-K-ATPase. Rb reabsorption was significantly increased after exposure to 10% CO(2) in CCD, and this effect was persistent for the entire 10% CO(2) period, whereas 10 microM SCH-28080 in the perfusate totally abolished the stimulation of Rb reabsorption by 10% CO(2). After stimulation of Rb reabsorption by 10% CO(2), subsequent addition of 0.1 mM methazolamide, an inhibitor of carbonic anhydrase, failed to affect Rb reabsorption. However, simultaneous exposure to 10% CO(2) and methazolamide prevented the stimulation of Rb reabsorption. Treatment with the intracellular calcium chelator MAPTAM (0.5 microM) inhibited the stimulation of Rb reabsorption by 10% CO(2). Similar inhibition was also observed in the presence of either a calmodulin inhibitor, W-7 (0.5 microM), or colchicine (0.5 mM), an inhibitor of tubulin polymerization. In time control studies, the perfusion time did not significantly affect Rb reabsorption. We conclude the following: 1) stimulation of Rb reabsorption on exposure to 10% CO(2) is dependent on the presence of a functional H-K-ATPase and appears to be regulated in part by the insertion of this enzyme into the apical plasma membrane by exocytosis; 2) insertion of H-K-ATPase requires changes in intracellular pH and needs a basal level of intracellular calcium concentration; and 3) H-K-ATPase insertion occurs by a microtubule-dependent process.

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MEDLINE

1931-857X

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F366-73

pubmed-meshheading:11457729-Absorption, pubmed-meshheading:11457729-Animals, pubmed-meshheading:11457729-Carbon Dioxide, pubmed-meshheading:11457729-Chelating Agents, pubmed-meshheading:11457729-Colchicine, pubmed-meshheading:11457729-Diuretics, pubmed-meshheading:11457729-Egtazic Acid, pubmed-meshheading:11457729-Enzyme Inhibitors, pubmed-meshheading:11457729-Female, pubmed-meshheading:11457729-Gout Suppressants, pubmed-meshheading:11457729-H(+)-K(+)-Exchanging ATPase, pubmed-meshheading:11457729-Imidazoles, pubmed-meshheading:11457729-Kidney Tubules, Collecting, pubmed-meshheading:11457729-Methazolamide, pubmed-meshheading:11457729-Perfusion, pubmed-meshheading:11457729-Potassium, pubmed-meshheading:11457729-Rabbits, pubmed-meshheading:11457729-Rubidium, pubmed-meshheading:11457729-Sulfonamides

Increased CO(2) stimulates K/Rb reabsorption mediated by H-K-ATPase in CCD of potassium-restricted rabbit.

Journal Article, In Vitro, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S.