Control of descending vasa recta pericyte membrane potential by angiotensin II.
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 microM) 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 microM) or removal of extracellular Ca(2+). 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 Ca(2+)-dependent Cl(-) conductance in OMDVR pericytes to induce membrane depolarization and Psi m oscillations.[1]References
- Control of descending vasa recta pericyte membrane potential by angiotensin II. Pallone, T.L., Huang, J.M. Am. J. Physiol. Renal Physiol. (2002) [Pubmed]
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