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Am J Physiol Renal Physiol 287: F1213-F1222, 2004. First published August 17, 2004; doi:10.1152/ajprenal.00241.2004
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Inhibition of K+ conductance in descending vasa recta pericytes by ANG II

Thomas L. Pallone, Chunhua Cao, and Zhong Zhang

Division of Nephrology, Department of Medicine, and Department of Physiology, University of Maryland School of Medicine, Baltimore, Maryland 21201-1595

Submitted 28 June 2004 ; accepted in final form 9 August 2004

We tested whether K+ channel inhibition accompanies ANG II-induced depolarization of descending vasa recta (DVR) pericytes. An increase in extracellular K+ concentration ([K+]o) from 5 to 100 mM depolarized resting pericytes but had no effect after prolonged (10 nM, 20 min) ANG II exposure. In contrast, reduction of extracellular Cl– concentration ([Cl–]o) from 154 to 34 mM had a minor effect on resting membrane potential but strongly depolarized pericytes treated with ANG II. The K+ channel blockers BaCl2 (0.1, 1 mM) and tetraethylammonium (TEA; 30 mM) depolarized resting pericytes but did not affect membrane potential of ANG II-treated pericytes. Pericyte whole cell currents were reduced by ANG II and nearly eliminated by combined ANG II exposure and the Cl– channel blocker niflumic acid (100 µM). Augmentation of inward current induced by raising [K+]O from 5 to 50 mM was eliminated by preexposure to ANG II. TEA- and BaCl2-sensitive outward currents, generated by depolarizing pericytes from –80 to –40 mV, were eliminated by ANG II. We conclude that ANG II depolarizes DVR pericytes by a combination of Cl– channel activation and K+ channel inhibition.

patch clamp; microcirculation; kidney; medulla


Address for reprint requests and other correspondence: T. L. Pallone, Div. of Nephrology, N3W143, Univ. of Maryland at Baltimore, 22 S. Green St., Baltimore, MD 21201-1595 (E-mail: tpallone{at}medicine.umaryland.edu)




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