The Inhibition Role And Its Mechanism Of Nitric Xoide On Myocardial Hypertrophy Induced By Angâ…¡ In Cultured Neonatal Rat Cardiomyocytes

Objective: To observe the role of NO on Angâ…¡-induced myocardial hypertrophy and its signal transduction pathway of PKC in cultured neonatal rat cardioymyocytes. Method: Set up myocardial hypertrophy model in primary cultured neonatal rat cardiomyocytes, the cell surface area, protein content, and the 3H-leucine incorporation were chose as indicators. Results: The cell surface area, protein content, and the 3H-leucine incorporation could be significantly increased by Angll in a dose-dependent manner, while pretreatment saralasin, pertussis toxin (PTX), and staurosporine could inhibit the effect of Angll on the promotion of 3H-leucine incorporation respectively; without Angll, each of them had no effect on 3H-leucine incorporation. L-arginine significantly decreased 3H-leucine incorporation and mRNA expression of ANF, and also could abolish the effect of cardiac hypertrophy induced by Ang II; These effects were inhibited by L-NAME, a NOS blocker. 3H-leucine incorporation and mRNA expression of ANF were significantly augmented by PMA, a PKC activator, in cultured neonatal rat cardiomyocytes. The effect can be decreased by NO precursor L-Arg but strengthened by L-NAME. In addition, mRNA expression of ANF was abolished by sodium nitroprusside (SNP), an exogenous NO donor. SNP could also restrain mRNA expression of ANF that was increased by Ang II. conclusions: The mechanism of Ang II-induced cardiomyocyte hypertrophic was linked with Ang II receptor and PTX sensitive G protein; PKC can inhibit the activeness of NOS, it suggested that PKC may be involved in the process of NO's preventing cardiac hypertrophy induced by Ang II in cultured neonatal rat cardiomyocytes.