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目的：探讨ＳＨＲ大鼠主动脉平滑肌细胞（ＡＳＭＣ）异常增殖和肾素血管紧张素系统（ＲＡＳ）的关系．方法：测定血管紧张素Ｉ（Ａｎｇ）、卡托普利（Ｃａｐ）、沙拉新（Ｓａｒ）对培养的ＳＨＲ、ＷＫＹＡＳＭＣ增殖和Ａｎｇ、血管紧张素转化酶（ＡＣＥ）的影响．结果：Ａｎｇ在２％血清培养基中可刺激ＳＨＲＡＳＭＣ增生．ＳＨＲＡＳＭＣ分裂增殖能力比ＷＫＹ强，ＳＨＲＡＳＭＣＲＡＳ处于高功能状态．Ｃａｐ长期（４周）干预显著抑制ＳＨＲＡＳＭＣ异常增殖和Ａｎｇ、ＡＣＥ活性，Ｓａｒ长期干预同样抑制ＳＨＲＡＳＭＣ的增殖和ＡＣＥ活性，但Ａｎｇ水平反而升高．Ｃａｐ短期（２４小时）干预不影响两种大鼠ＡＳＭＣＲＡＳ．结论：Ｃａｐ和Ｓａｒ长期干预通过减少ＳＨＲＡＳＭＣＡｎｇ生成或阻断Ａｎｇ和特异受体结合，抑制其异常增殖．
Objective: To investigate the relationship between abnormal proliferation of aortic smooth muscle cells (ASMCs) and renin-angiotensin system (RAS) in SHR rats. Methods: The effects of angiotensin I (Ang), Cap and Sar on proliferation of cultured SHR and WKYASMC and Ang and angiotensin converting enzyme (ACE) were measured. RESULTS: Ang 2 stimulated SHRASMC hyperplasia in 2% serum medium. SHRASMC has stronger division and proliferation ability than WKY and SHRASMCRAS is highly functional. Cap long-term (4 weeks) intervention significantly inhibited the abnormal proliferation and angiotensin-converting enzyme activity of SHRASMC. Sar long-term intervention also inhibited the proliferation and ACE activity of SHRASMC, but Ang increased. Cap short-term (24 h) intervention did not affect both rat ASMCRAS. Conclusion: Long-term intervention by Cap and Sar inhibits the abnormal proliferation of SHRASMCAng by decreasing the binding of Ang and specific receptors.