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蛋白激酶C在血管紧张素Ⅱ抑制心肌细胞一氧化氮合成中的作用

符史干, 刘培庆, 鲁伟, 龚素珍, 潘敬运

中山医科大学生理教研室.广东,广州 510080

摘要

AngⅡ可减少心肌细胞NO的含量,并具有明显的剂量-效应关系;AngⅡ受体拮抗剂saralasin可明显抑制AngⅡ对NO生成的影响;L-精氨酸(L-Arg)明显增加心肌细胞NO的浓度,此效应可被一氧化氮合酶(NOS)抑制剂L-NAME所抑制,L-Arg未能消除AngⅡ抑制NO的作用;用佛波酯(PMA)处理心肌细胞,其NO的生成明显减少,L-NAME可加强此抑制效应;PKC抑制剂staurosporine(Stau)可明显削弱AngⅡ抑制心肌细胞NO生成的效应。

Effect of protein kinase C on inhibition of nitric oxide synthesis in cultured neonatal rat cardiomyocytes by angiotensin II

Fu Shigan, Liu Peiqing, Lu Wei, Gong Suzhen, Pan Jingyun

Department of Physiology,Sun Yat-Sen University of Medical Sciences.Guangzhou 510080,Guangdong

Abstract

NO production was decreased by Ang II in a dose-dependent manner but increased by L-Arg. The Saralasin, an antagonist of AngII receptor, inhibited the effect of AngII on NO production. The effect of AngII on NO production was inhibited by NOS blocker N~(G)-nitro-L-arginine methyl ester (L-NAME) but not by L-Arg. Pretreatment of Phorbol 12-myristate 13-acetate (PMA), a PKC activator, decreased NO concentration significantly. This effect was strengthened by L-NAME. Staurosporine, a PKC inhibitor, abolished the inhibiting effect of AngII on production of NO.

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引用本文：

符史干, 刘培庆, 鲁伟, 龚素珍, 潘敬运. 蛋白激酶C在血管紧张素Ⅱ抑制心肌细胞一氧化氮合成中的作用[J]. 生理学报 2000; 52 (4): .

Fu Shigan, Liu Peiqing, Lu Wei, Gong Suzhen, Pan Jingyun. Effect of protein kinase C on inhibition of nitric oxide synthesis in cultured neonatal rat cardiomyocytes by angiotensin II. Acta Physiol Sin 2000; 52 (4): (in Chinese with English abstract).