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一氧化氮在血管紧张素且激活蛋白激酶C中的作用

符史干, 谢协驹, 吉丽敏, 刘培庆, 潘敬运, 鲁伟

海南医学院生理教研室，海口571101

摘要

实验在培养新生大鼠心肌细胞中检测N。前体L一精氨酸(L- Arg)和N。供体硝普钠(SNP)对血管紧张素Ⅱ( Ang 11)激活蛋白激酶C (PKC)的作用，以探讨心肌细胞PKC水平的信号转导途径。实验结果如下:(1)无血清DMEM培养心肌细胞24 h后加入Ang Ⅱ，P KC活性呈剂量依赖性增高;(2)培养基中加入L-Arg, P KC活性呈剂量依赖性降低;(3)用L-Arg 100 umol/ L进行预处理，30 min后分别加入Ang Ⅱ 0.1 umol/ L或P MA 1 0
umol/L, PKC活性均明显降低，与单纯Ang 11组和单纯PMA组相比均有显著性差异;用NOS抑制剂L-NAME预处理后，再加入L-Arg，可明显阻断L-Arg对上述两个效应的影响;(4)培养液中加入N。供体SNP, PKC活性呈剂量依赖性地降低;(5)用SNP 10 umol/ L预处理心肌细胞，5 min后分别加入Ang Ⅱ或PMA, PKC活性分别与单纯Ang 11和单纯PMA组相比均明显降低。以上结果表明，Ang Ⅱ能剂量依赖性激活PKC，而N。可剂量依赖性抑制PKC活性;NOS参与L- Arg抑制Ang 11或PMA激活P KC的作用。这些观察提示，NO抑制Ang 11对心肌细胞的作用可能是通过抑制PKC活性实现的，PKC可能是N。和Ang Ⅱ在心肌细胞内信号转导的交汇点(crosstalk).

关键词： 心肌细胞培养; 血管紧张素Ⅱ; 一氧化氮; 蛋白激酶C

Influence of nitric oxide on the angiotensin Ⅱ一activated protein kinase C activaty in cultured neonatal rat cardiomycytes

FU SHi-GAN, XIE Xie- Ju, JILi- Min, LIU Pei Qing, PAN Jing Yun, Lu Wei

Department of Physiology, Hainan Medical College, Haikou 571101；Department of Physiology Sun Yat-Sen University of Medical Sciences，Guangzhou 510089

Abstract

We examined the effect of endogenous and exogenous nitric oxide(NO) on protein kinase C(PKC) activity induced by angiotensin Ⅱ(Ang Ⅱ)in cultured neonatal rat cardiomyocytes .The results are as follows .The activity of PKC was increased by Ang Ⅱ(0. 01一10 p mol/ L) in a dose-dependent manner，but decreased by NO precursor L一arginine(L一Arg)(10 umol/ L一1 0 m mol/ L) in a
dose-dependent manner in cultured neonatal rat cardiomyocytes .Pretreatment with L一Arg(100 umol/L) decreased significantly Ang 1I一activated PKC activity and PKC activity induced by phorbol 12myristate 13-acetate(P MA)(10 pmol/L)，a PKC activator.Pretreatment with N(}-nitro- L-argingie methyl ester(L一NAME)，a nitric oxide synthase(NOS) Mocker，may inhibit significantly the role of
L一Arg on Ang Ⅱ一and P MA activated P KC activity .The activity of PKC was also decreased by NO donor sodium nitroprusside(S NP)(10 umol/L一1 mmol/ L) in a dose-dependent manner in cultured neonatal rat cardiomyocytes .Pretreatment with SNP(1 0 p mol/ L) decreased significantly AngⅡ一and P MA activated P KC activity.These results indicate that PKC was controlled by both NO and Ang Ⅱ.
PKC may be a“cross talk" between Ang Ⅱ and NO in cardiomyocytes .NO abolished the activity of PKC and impaired PKC downstream signaling transduction pathway cascades.

Key words: neonatal rat myocardial cell culture;angiotensinⅡ;;

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引用本文：

符史干, 谢协驹, 吉丽敏, 刘培庆, 潘敬运, 鲁伟. 一氧化氮在血管紧张素且激活蛋白激酶C中的作用[J]. 生理学报 2003; 55 (1): .

FU SHi-GAN, XIE Xie- Ju, JILi- Min, LIU Pei Qing, PAN Jing Yun, Lu Wei. Influence of nitric oxide on the angiotensin Ⅱ一activated protein kinase C activaty in cultured neonatal rat cardiomycytes. Acta Physiol Sin 2003; 55 (1): (in Chinese with English abstract).