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.