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Am J Physiol Regul Integr Comp Physiol 283: R949-R957, 2002. First published June 27, 2002; doi:10.1152/ajpregu.00251.2002
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Vol. 283, Issue 4, R949-R957, October 2002

Membrane potential controls calcium entry into descending vasa recta pericytes

Zhong Zhang, Kristie Rhinehart, and Thomas L. Pallone

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

We tested the hypothesis that constriction of descending vasa recta (DVR) is mediated by voltage-gated calcium entry. K+ channel blockade with BaCl2 (1 mM) or TEACl (30 mM) depolarized DVR smooth muscle/pericytes and constricted in vitro-perfused vessels. Pericyte depolarization by 100 mM extracellular KCl constricted DVR and increased pericyte intracellular Ca2+ ([Ca2+]i). The KATP channel opener pinacidil (10-7-10-4 M) hyperpolarized resting pericytes, repolarized pericytes previously depolarized by ANG II (10-8 M), and vasodilated DVR. The DVR vasodilator bradykinin (10-7 M) also reversed ANG II depolarization. The L-type Ca2+ channel blocker diltiazem vasodilated ANG II (10-8 M)- or KCl (100 mM)-preconstricted DVR, and the L-type agonist BayK 8644 constricted DVR. The plateau phase of the pericyte [Ca2+]i response to ANG II was inhibited by diltiazem. These data support the conclusion that DVR vasoreactivity is controlled through variation of membrane potential and voltage-gated Ca2+ entry into the pericyte cytoplasm.

medulla; kidney; microcirculation; patch clamp; fura-2; KCl


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