一氧化氮在血管紧张素Ⅱ诱导心肌细胞肥大中的作用

在培养新生大鼠心肌细胞上，探讨一氧化氮（ＮＯ）在血管紧张素Ⅱ诱导的心肌细胞以大中的作用。结果显示，血管紧张素Ⅱ可使心肌细胞蛋白质含量显著增加，心肌细胞一氧化氮合酶（ＮＯＳ）活性和培养液ＮＯ浓度明显降低。血管紧张素Ⅱ可明显降低心肌细胞ｅＮＯＳｍＲＮＡ水平。Ｓａｒａｌｓｉｎ和百日咳毒素（ＰＴＸ）可抑制血管紧张素Ⅱ诱导的蛋白质含量增加、心肌细胞ＮＯＳ活性减弱和培养液ＮＯ浓度降低。硝普钠提高心肌细胞培养

The role of nitric oxide in the angiotensin II-induced hypertrophy of cardiac myocytes

The purpose of this study was to determine the role of nitric oxide (NO) in the angiotensin II-induced hypertrophic response in cultured neonatal rat cardiac myocytes. Angiotensin II induced significant increase of protein content, decrease of NOS activity in cultured neonatal rat cardiomyocytes and decrease of NO concentration in the culture medium. Angiotensin II decreased significantly the eNOS mRNA level of cardiomyocytes. Saralasin and PTX inhibited significantly the increased protein content, the decreased NOS activity and the decreaseed NO production of cardiomyocytes induced by angiotensin II. Sodium nitroprusside increased significantly NO concentration in the culture medium and inhibited significantly the increased protein content of cardiomyocytes induced by angiotensin II. The results suggest that angiotensin II may induce hypertrophy of cultured neonatal rat cardiomyocytes. The effect of angiotensin II is mediated by receptors which are coupled with PTX-sensitive G protein and may be related to the decreased eNOS gene expression, NOS activity and NO production. Exogenous NO can prevent the hypertrophy of cardiomyocytes induced by angiotensin II.