蛋白激酶C在血管紧张素Ⅱ抑制心肌细胞——氧化氮合成中的作用

实验用硝酸还原酶法测定培养新生大鼠内肌细胞亚硝酸盐（ＮＯ２）和硝酸盐（ＮＯ３）总量（ＮＯ２／ＮＯ３）,反映心肌细胞一氧化氮（ＮＯ）生成情况,观察血管紧张素Ⅱ（ＡｎｇⅡ）对凡肌细胞ＮＯ生成的及其蛋白激酶Ｃ（ＰＫＣ）在该效应中的作用。结果显示：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可明显抵制ＡｎｇⅡ对ＮＯ生成的影响;Ｌ－精氨酸（Ｌ－Ａｒｇ）明

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

The purpose of the present study was to investigate the effect of angiotensin II (Ang II) on nitric oxide (NO) concentration and its signal transduction pathway in cultured neonatal rat cardioymocytes. NO content was measured in cultured neonatal rat cardiomyoctes using a nitrite/nitrate colormetric method kit. NO content was represented by measured nitrite (NO(2)) and nitrate (NO(3)) level (NO(2)/NO(3)). The results are as follows. NO production was decreased by Ang II in a dose dependent manner but increased by L Arg. The Saralasin, an antagonist of Ang II receptor, inhibited the effect of Ang II on NO production. The effect of Ang II 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 Ang II on production of NO. The above results suggest that Ang II could decrease NO content in cultured neonatal rat cardiomyocytes significantly. Activity of NOS may be inhibited by Ang II. Ang II receptor was involved in the inhibitory effect of Ang II on NO production. Activation of protein kinase C (PKC) decreased significantly NO production in cultured neonatal rat cardiomyoctes, which appears to be associated with PKC in the signal transduction pathway.