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Am J Physiol Renal Physiol 282: F1064-F1074, 2002. First published January 29, 2002; doi:10.1152/ajprenal.00306.2001
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Vol. 282, Issue 6, F1064-F1074, June 2002

Control of descending vasa recta pericyte membrane potential by angiotensin II

Thomas L. Pallone and James M.-C. Huang

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

Using nystatin perforated-patch whole cell recording, we investigated the role of Cl- conductance in the modulation of outer medullary descending vasa recta (OMDVR) pericyte membrane potential (Psi m) by ANG II. ANG II (10-11 to 10-7 M) consistently depolarized OMDVR and induced Psi m oscillations at lower concentrations. The Cl- channel blockers anthracene-9-decarboxylate (1 mM) and niflumic acid (10 µM) hyperpolarized resting pericytes and repolarized ANG II-treated pericytes. In voltage-clamp experiments, ANG II-treated pericytes exhibited slowly activating currents that were nearly eliminated by treatment with niflumic acid (10 µM) or removal of extracellular Ca2+. Those currents reversed at -31 and -10 mV when extracellular Cl- concentration was 152 and 34 mM, respectively. In pericytes held at -70 mV, oscillating inward currents were sometimes observed; the reversal potential also shifted with extracellular Cl- concentration. We conclude that ANG II activates a Ca2+-dependent Cl- conductance in OMDVR pericytes to induce membrane depolarization and Psi m oscillations.

medulla; kidney; microcirculation; patch clamp; niflumic acid; oscillations


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