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Am J Physiol. 1996 Mar;270(3 Pt 2):F539-47.

Stimulation of apical H-K-ATPase in intercalated cells of cortical collecting duct with chronic metabolic acidosis.

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1
Department of Physiology, Cornell University Medical College, New York 10021, USA.

Abstract

This study evaluated the role of H-K-adenosinetriphosphatase (H-K-ATPase) with chronic metabolic acidosis (CMA) in intercalated cells (ICs) of rabbit cortical collecting duct (CCD). CMA was induced by replacing drinking water with 75 mM NH4Cl in 5% sucrose for 10-14 days. CCDs isolated from CMA and control rabbits were split open and exposed to the intracellular pH (pHi) indicator 2',7'-bis(carboxyethyl)-5(6)-carboxyfluorescein. In N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid-buffered solutions, the resting pHi in ICs was similar for both groups. K-dependent pHi recovery (5 mM K, 140 mM N-methyl-D-glucamine) was monitored in response to a pulse of NH4Cl (10 mM). The K-dependent pHi recovery rate was threefold higher in CMAICs compared with controls and was abolished with the gastric H-K-ATPase inhibitor, Sch-28080 (10(-5) M). Polarity of the H-K-ATPase was studied in microperfused CMA and control CCDs. Luminal K-dependent pHi recovery was monitored in response to an acute pulse of NH4Cl in individual peanut lectin agglutinin (PNA)-binding ICs. The apical Sch-28080-inhibitable K-dependent pHi recovery rate was significantly greater in CMA ICs than control ICs. In summary, CMA enhances functional activity of an apical H-K-ATPase in PNA-binding ICs of rabbit CCD.

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