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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。
To culture neonatal rat cardiomyocytes as a model, the inhibitory effect of captopril on cardiomyocyte growth was observed. Captopril 20 and 200umol·L ~ (-1) in the cells 72h, the total protein content of myocardial cells decreased by 9% and 18%. However, no significant changes in the number of cells. With [~ 3H] leucine binding method, measured angiotensin Ⅱ 1, 10.100nmol·L ~ (-1) increased protein synthesis in 48h 29%. 53% and 70%, but with [~ 3H] thymidine incorporation of DNA synthesis measured no significant increase. Captopril 20 and 200 μmol·L ~ (-1) decreased the protein synthesis of cells regardless of the presence of 100 nmol·L -1 angiotensin Ⅱ. The results suggest that captopril can directly inhibit the growth of cardiomyocytes. This effect may be related to its inhibition of myocardial hypertrophy.