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Articles in PresS, published online ahead of print June 27, 2002
Am J Physiol Regu Physiol, 10.1152/ajpregu.00251.2002
Submitted on May 6, 2002
Accepted on June 24, 2002
1 Division of Nephrology, University of Maryland School of Medicine, Baltimore, MD, USA
* To whom correspondence should be addressed. E-mail: tpallone{at}medicine.umaryland.edu.
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 angiotensin II (AngII, 10-8 M) and vasodilated DVR. The DVR vasodilator, bradykinin (10-7 M), also reversed AngII depolarization. The L type Ca2+ channel blocker, diltiazem, vasodilated AngII (10-8 M) or KCl (100 mM) preconstricted DVR and the L type agonist BAYK8644 constricted DVR. The plateau phase of the pericyte [Ca2+]i response to AngII 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.
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