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Molecular mechanism of nitric oxide in preventing cardiomyocytes from hypertrophic response induced by angiotensin Ⅱ

Liu Peiqing, Lu Wei, Pan Jingyun

Department of Physiology,Sun Yat-Sen University of Medical Sciences.Guangzhou 510089,Guangdong

Abstract

The results are as follows. (1) L-arginine (L-Arg) induced a dose-dependent increase in NO by 16% and 31% at the concentrations of 10 #mu#mol/L and 100 #mu#mol/L, respectively. L-Arg also increased the gene expression of eNOS. However, these effects were inhibited by L-NAME, the inhibitor of NOS. (2) The gene expression and the protein synthesis of ANP induced by Ang II (0.1 #mu#mol/L) were inhibited by L-Arg (100 #mu#mol/L). The inhibitory action of L-Arg was abolished after pretreatment with antisense oligoneucleotide against MKP-1. (3) L-Arg (100#mu#mol/L) increased the protein expression of MKP-1 by 225%, which was inhibited by L-NAME, an NOS inhibitor, and KT-5823, a cGMP-dependent protein kinase (PKG) inhibitor. However, Ang II enhanced the effect induced by L-Arg.

Key words: Mitogeiractivated protein kinase phosphatase-1;Cyclic GMP-dependent protein kinases;Cardiomyocyte;Hypertrophy;Angiotensin II;Nitric oxide;Arginine

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Citing This Article：

Liu Peiqing, Lu Wei, Pan Jingyun. Molecular mechanism of nitric oxide in preventing cardiomyocytes from hypertrophic response induced by angiotensin Ⅱ. Acta Physiol Sin 2002; 54 (3): (in Chinese with English abstract).