摘要
以培养乳鼠心肌细胞作为模型,观察了卡托普利对心肌细胞生长的抑制作风结果表明。卡托普利20和200umol·L ̄(-1)作用于细胞72h,心肌细胞的总蛋白质量分别减少9%和18%。但细胞数目未见明显变化。用[ ̄3H]亮氨酸结合的方法,测得血管紧张素Ⅱ1,10.100nmol·L ̄(-1)在48h内增加蛋白质合成29%。53%和70%,但用[ ̄3H]胸腺嘧啶核苷结合的方法测得DNA的合成未见明显增加。无论100nmol·L ̄(-1)血管紧张素Ⅱ是否存在,卡托普利20和200umol·L ̄(-1)均能够减少细胞的蛋白质合成。结果提示卡托普利可以直接抑制心肌细胞的生长。此作用可能与其抑制心肌肥厚有关。
By using myocardial cells in culture as amodel. the effccts of captopnl (Cap) on the growth of cardiacmyocytc were observed. The results showed that there was nosignificani change in cell number. but a significant decrease of9%. 18% in total cellular protein alter 72 h exposure to Cap20. 200 umol · L ̄(-1) . Forty-eight hours exposure to 1. 10. 100)nmol · L ̄(-1) angiotensin Ⅱ caused a 29%. 53%. 70% incrcascin protein synthesis as measured by [ ̄3H]leucine incorporation,but no significant change in DNA synthesis Cap 20. 200ymol · L ̄(-1) were able to reduce the protein synthesis in thepresence and absence of 100 nmol · L ̄(-1) angiotensin Ⅱ. The re-sults suggested that the direct inhibitory action of Cap on thegrowth of myocytes may bc rclated to the cardiachyperi rophy。
出处
《中国药理学与毒理学杂志》
CAS
CSCD
北大核心
1995年第1期8-11,共4页
Chinese Journal of Pharmacology and Toxicology
关键词
心肌
卡托普利
血管紧张素Ⅱ
乳鼠
药理
cells. cultured, myocardium,captopnl, angiotensin Ⅱ. kininase Ⅱ, hypertrophy,myocardium