ANG II signaling in vasa recta pericytes by PKC and reactive oxygen species.
ANG II signaling in vasa recta pericytes by PKC and reactive oxygen species.
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PKC 和活性氧在直肠血管周细胞中的 ANG II 信号传导。
DOI：
10.1152/ajpheart.01135.2003
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发表时间：
2004
期刊：
影响因子：
--
通讯作者：
Pallone,ThomasL
中科院分区：
文献类型：
--
作者：
Zhang,Zhong;Rhinehart,Kristie;Kwon,Whaseon;Weinman,Edward;Pallone,ThomasL
血管紧张素II通过周细胞中的Ca 2+信号收缩直小血管（DVR）。我们研究了从大鼠肾脏外髓质分离的PKC DVR周细胞的作用。PKC阻断剂staurosporine（10 μM）消除ANG II（10 nM）诱导的血管收缩，抑制周细胞胞质Ca 2+浓度（[Ca 2 +]cyt）升高，并阻断Mn 2+流入胞质。用1，2-二辛酰甘油（10 μM）或佛波醇1,2，13-二丁酸酯（PDBu; 1 μM）激活PKC可引起血管收缩和周细胞[Ca ~（2+）]升高。地尔硫卓（10 μM）阻断PDBu增加周细胞[Ca ~（2+）]细胞和增加Mn ~（2+）内流的能力。ANG II和PDBu-induced PKC刺激DVR产生的活性氧（ROS），测量氧化的二氢乙锭（DHE）。仅当用PD-123319（10 nM）阻断ANG II AT 2受体时，ANG II的作用才显著。PDBu对DHE氧化的增强作用可被TEMPOL（1 mM）或二亚苯基碘鎓（10 μM）阻断。我们得出结论，ANG II和PKC激活增加DVR周细胞[Ca 2 +]细胞，二价离子电导进入细胞质，和ROS的产生。
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+]cytelevation. Diltiazem (10 μM) blocked the ability of PDBu to increase pericyte [Ca2+]cytand 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 AT2receptors 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.
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