Angiotensin II activates H+-ATPase in type A intercalated cells.
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(-)/HCO(3)(-) exchange as well as generates more favorable electrochemical gradient for ENaC-mediated Na(+) absorption.
Pech
Vladimír
V
Emory University School of Medicine, Renal Division, 1639 Pierce Drive, NE, WMB Room 338, Atlanta, GA 30322, USA. vpech@emory.edu
Zheng
Wencui
W
Pham
Truyen D
TD
Verlander
Jill W
JW
Wall
Susan M
SM
D000804:Angiotensin II / Q000494:pharmacology*; D000818:Animals; D004789:Enzyme Activation / Q000187:drug effects; D005665:Furosemide / Q000494:pharmacology*; D007672:Kidney Cortex / Q000187:drug effects / Q000502:physiology*; D007685:Kidney Tubules, Collecting / Q000187:drug effects / Q000502:physiology*; D051379:Mice; D006180:Proton-Translocating ATPases / Q000378:metabolism*
D000804:Angiotensin II; D005665:Furosemide; D006180:Proton-Translocating ATPases