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Am J Physiol Heart Circ Physiol 287: H773-H781, 2004. First published April 8, 2004; doi:10.1152/ajpheart.01135.2003
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ANG II signaling in vasa recta pericytes by PKC and reactive oxygen species

Zhong Zhang, Kristie Rhinehart, Whaseon Kwon, Edward Weinman, and Thomas L. Pallone

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

Submitted 1 December 2003 ; accepted in final form 5 April 2004

ANG II constricts descending vasa recta (DVR) through Ca2+ signaling in pericytes. We examined the role of PKC DVR pericytes isolated from the rat renal outer medulla. The PKC blocker staurosporine (10 µM) eliminated ANG II (10 nM)-induced vasoconstriction, inhibited pericyte cytoplasmic Ca2+ concentration ([Ca2+]cyt) elevation, and blocked Mn2+ influx into the cytoplasm. Activation of PKC by either 1,2-dioctanoyl-sn-glycerol (10 µM) or phorbol 12,13-dibutyrate (PDBu; 1 µM) induced both vasoconstriction and pericyte [Ca2+]cyt elevation. Diltiazem (10 µM) blocked the ability of PDBu to increase pericyte [Ca2+]cyt and enhance Mn2+ influx. Both ANG II- and PDBu-induced PKC stimulated DVR generation of reactive oxygen species (ROS), measured by oxidation of dihydroethidium (DHE). The effect of ANG II was only significant when ANG II AT2 receptors were blocked with PD-123319 (10 nM). PDBu augmentation of DHE oxidation was blocked by either TEMPOL (1 mM) or diphenylene iodonium (10 µM). We conclude that ANG II and PKC activation increases DVR pericyte [Ca2+]cyt, divalent ion conductance into the cytoplasm, and ROS generation.

medulla; kidney; microcirculation; calcium; oxidative stress


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




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