卡托普利对培养乳鼠心肌细胞蛋白质合成的抑制作用

Inhibitory effects of captopril on protein synthesis ofcultured neonatal rat heart cells

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。