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Angiotensin II Activates H⁺-ATPase in Type A Intercalated Cells

Vladimír Pech^*,, Wencui Zheng^,, Truyen D. Pham^*, Jill W. Verlander and Susan M. Wall^*,

^* Renal Division, Department of Medicine, and Department of Physiology, Emory University School of Medicine, Atlanta, Georgia; and Division of Nephrology, Hypertension, and Transplantation, Department of Medicine, University of Florida College of Medicine, Gainesville, Florida; V.P. and W.Z. contributed equally this work

Correspondence: Dr. Vladimir Pech, Emory University School of Medicine, Renal Division, 1639 Pierce Drive, NE, WMB Room 338, Atlanta, GA 30322. Phone: 404-727-2797; Fax: 404-727-3425; E-mail: vpech{at}emory.edu

Received for publication March 6, 2007. Accepted for publication July 27, 2007.

We reported previously that angiotensin II (AngII) increases net Cl^– absorption in mouse cortical collecting duct (CCD) by transcellular transport across type B intercalated cells (IC) via an H⁺-ATPase–and pendrin-dependent mechanism. Because intracellular trafficking regulates both pendrin and H⁺-ATPase, we hypothesized that AngII induces the subcellular redistribution of one or both of these exchangers. To answer this question, CCD from furosemide-treated mice were perfused in vitro, and the subcellular distributions of pendrin and the H⁺-ATPase were quantified using immunogold cytochemistry and morphometric analysis. Addition of AngII in vitro did not change the distribution of pendrin or H⁺-ATPase within type B IC but within type A IC increased the ratio of apical plasma membrane to cytoplasmic H⁺-ATPase three-fold. Moreover, CCDs secreted bicarbonate under basal conditions but absorbed bicarbonate in response to AngII. In summary, angiotensin II stimulates H⁺ secretion into the lumen, which drives Cl^– absorption mediated by apical Cl^–/HCO₃^– exchange as well as generates more favorable electrochemical gradient for ENaC-mediated Na⁺ absorption.

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