Proliferation of aortic smooth muscle cells and renin-angiotensin system in SHR rats

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．

Proliferation of aortic smooth muscle cells and renin-angiotensin system in SHR rats

AIM: To study the relationship between the enhanced proliferation and renin angiotensin system (RAS) of aortic smooth muscle cells (ASMC) from SHR rats. METHODS: To measure the effects of angiotensin II (Ang), captopril (Cap), saralasin (Sar) on proliferation, Ang and angiotensin converting enzyme (ACE) levels in cultured ASMC from WKY and SHR rats. RESULTS: Ang was a bifunctional growth factor, which induced SHR ASMC hyperplasia in 2 % FCS RPMI 1640 medium, but not in serum free (SF) medium. SHR ASMC had stronger proliferative ability compared with WKY while SHR ASMC RAS was activated. Enhanced proliferation of SHR ASMC and ACE activity were obviously inhibited by long term treatment (4 wk) of both Cap and Sar, while Ang content decreased in Cap treatment group and increased in Sar treatment group. The antiproliferative effect of Cap and Sar on SHR ASMC was stronger than that on WKY. SHR, WKY ASMC RAS were not influenced by short term (24 h) treatment of Cap. CONCLUSION: Long term treatment of Cap and Sar suppressed SHR ASMC growth through inhibition of Ang generation or blockade of Ang binding to its receptor.