ANG II signaling in vasa recta pericytes by PKC and reactive oxygen species

被引:35
作者
Zhang, Z
Rhinehart, K
Kwon, W
Weinman, E
Pallone, TL
机构
[1] Univ Maryland, Sch Med, Dept Med, Div Nephrol, Baltimore, MD 21201 USA
[2] Univ Maryland, Sch Med, Dept Physiol, Div Nephrol, Baltimore, MD 21201 USA
来源
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY | 2004年 / 287卷 / 02期
关键词
medulla; kidney; microcirculation; calcium; oxidative stress;
D O I
10.1152/ajpheart.01135.2003
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
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 muM) 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 muM) or phorbol 12,13-dibutyrate (PDBu; 1 muM) induced both vasoconstriction and pericyte [Ca2+](cyt) elevation. Diltiazem (10 muM) 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 AT(2) receptors were blocked with PD-123319 (10 nM). PDBU augmentation of DHE oxidation was blocked by either TEMPOL (1 mM) or diphenylene iodonium (10 muM). We conclude that ANG II and PKC activation increases DVR pericyte [Ca2+] divalent ion conductance into the cytoplasm, and ROS generation.
引用
收藏
页码:H773 / H781
页数:9
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