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实验用硝酸还原酶法测定培养新生大鼠心肌细胞亚硝酸盐 (NO 2 )和硝酸盐 (NO 3)总量 (NO 2 /NO 3) ,反映心肌细胞一氧化氮 (NO)生成情况 ,观察血管紧张素Ⅱ (AngⅡ )对心肌细胞NO生成的影响及其蛋白激酶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可明显抑制AngⅡ对NO生成的影响 ;L 精氨酸 (L Arg)明显增加心肌细胞NO的浓度 ,此效应可被一氧化氮合酶 (NOS)抑制剂L NAME所抑制 ,L Arg未能消除AngⅡ抑制NO的作用 ;用佛波酯 (PMA)处理心肌细胞 ,其NO的生成明显减少 ,L NAME可加强此抑制效应 ;PKC抑制剂staurosporine (Stau)可明显削弱AngⅡ抑制心肌细胞NO生成的效应。结果提示 :AngⅡ具有抑制心肌细胞NO生成的作用 ,此作用可能是通过抑制心肌细胞NOS的活性而实现的 ;AngⅡ受体介导AngⅡ抑制心肌细胞NO生成的作用 ;激活PKC可使新生大鼠心肌细胞NO生成减少 ,NOS参与此抑制效应 ,新生大鼠心肌细胞NO生成过程的信号转导通路可能与PKC有关 ;PKC参与AngⅡ抑制心肌细胞NO的生成。
The nitric oxide (NO 2) and nitric oxide (NO 3) contents of neonatal rat cardiomyocytes were measured by nitric acid reductase method, and the formation of nitric oxide (NO) in cardiomyocytes was observed. Effects of Ang Ⅱ on NO Production in Cardiomyocytes and the Role of Protein Kinase C (PKC) in this Effect. The results showed that: Ang Ⅱ can reduce the content of NO in cardiomyocytes, and have obvious dose-effect relationship; Ang Ⅱ receptor antagonist saralasin can significantly inhibit the effect of AngⅡ on NO production; L Arg significantly increases NO L Arg did not abolish the effect of Ang II on NO production. The production of NO was significantly reduced by treatment of cardiomyocytes with phorbol myristate (PMA), but this effect was inhibited by L NAME, a nitric oxide synthase (NOS) inhibitor. L NAME enhanced the inhibitory effect. Staurosporine (Stau), a PKC inhibitor, significantly attenuated the effect of AngII on NO production in cardiomyocytes. The results suggest that: Ang Ⅱ can inhibit the production of NO in cardiomyocytes, which may be through the inhibition of NOS activity in cardiomyocytes; AngⅡinduces AngⅡ to inhibit the production of NO in cardiomyocytes; NOS is involved in this inhibitory effect, and the signal transduction pathway of NO production in neonatal rat cardiomyocytes may be related to PKC; PKC may be involved in the inhibition of NO production by AngⅡin cardiomyocytes.