一氧化氮在血管紧张素Ⅱ诱导心肌细胞肥大中的作用
詹昌德, 王庭槐, 潘敬运
中山医科大学卫生部辅助循环重点实验室.广东,广州 510089;中山医科大学生理学教研室.广东,广州 510089
摘要
血管紧张素Ⅱ通过PTX敏感的G蛋白途径,诱导培养的新生大鼠心肌细胞肥大反应,该作用可能与血管紧张素Ⅱ抑制心肌细胞eNOS基因表达、NOS活性和NO生成有关;外源性NO可防止血管紧张素Ⅱ诱导的心肌细胞肥大反应。
The role of nitric oxide in the angiotensin II-induced hypertrophy of cardiac myocytes
Zhan Changde, Wang Tinghuai, Pan Jingyun
Department of Physiology,Sun Yat-sen University of Medical Sciences.Guangzhou 510089,Guangdong;Department of Physiology,Sun Yat-Sen University of Medical Sciences.Guangzhou 510089,Guangdong
Abstract
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.
Key words: Nitric oxide;Angiotensin Ⅱ;Hypertrophy of cardiac myocytes
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引用本文:
詹昌德, 王庭槐, 潘敬运. 一氧化氮在血管紧张素Ⅱ诱导心肌细胞肥大中的作用[J]. 生理学报 1999; 51 (6): .
Zhan Changde, Wang Tinghuai, Pan Jingyun. The role of nitric oxide in the angiotensin II-induced hypertrophy of cardiac myocytes. Acta Physiol Sin 1999; 51 (6): (in Chinese with English abstract).