Study on the protection by nitric oxide generated from L-Arginine

点击翻译按钮获取中文摘要

Protective effects of L-arginine were evaluated in a cardiomyocytes and endothels got from rats model of low-volume anoxia and re-oxygenation. Cell cultures were subjected to 90 min of low-volume anoxia and 30 min of re-oxygenation. L-Arginine (0-0.5 mM) was administered during the pre-anoxic period or the re-oxygenation phase. Nitric oxide (NO) production, NO synthase (NOS) activity, cGMP levels, and cellular injury were assessed. To evaluate the effects of the L-arginine on cell signaling, the effects of the NOS antagonist NG-nitro-L-arginine methyl ester (L-NAME), No donor S-nitroso-N-acetyl-penicillamine (SNAP), guanylate cyclase inhibitor methylene blue, cGMP analog 8-bromo-cGMP were examined. This data indicate that low-volume anoxia and re-oxygenation might increase NOS activity and facilitated the conversion of L-arginine to NO, which provided protection against cellular injury in a dose-dependent fashion. In addition, the cardioprotective effects of L-arginine were achived by the activation of guanylate cyclase, leading to increased cGMP levels in rat heart cells. This action involves a glibenclamide-sensitive, NO-cGMP-dependent pathway.