Aim To investigate the relationship between the enhanced proliferation and renin-angiotensin system (RAS) of aortic smooth muscle cells (SMC ) from spontaneously hypertensive rats .(SHR).Methods Proliferative activity of SMC was assessed by 3H-TdR incorporation and doubling time (DT).Angiotensin Ⅱ (Aug Ⅱ ) content and angiotensin converting enzyme (ACE) activity were measured by radioimmunoassay and colorimetry respectively.Results SHR SMC had stronger proliferative ability compared with Wistar-kyoto normotensive rats (WKY) while SHR SMC RAS was activated. Enhanced proliferation of SHR SMC was obviously inhibited with the long-term administration of captopril (Cap) and saralasin (Sar). The inhibition rate on HTdR incorporation of SHR SMC by 10-4 mol/L Cap was 31%±4% (p<0. 01 ) while the DT was prolonged for about 13 h (p<0. 01 ). Aug Ⅱ content and ACE activity were decreased for 25%±9%, 27%±13 % respectively. The inhibition rates on 3H-TdR incorporation of SHR SMC by 10-5 mol/L Sar was 20%±3% (p<0. 05) while the DT was prolonged for about 7 h (p<0. 05). The Aug I content that two types of rats synthesized and secreted increased while ACE activity of SHR SMC decreased by 10-s mol/L Sar.SHR, WKY SMC RAS were not influenced by shortterm administration of Cap.Conclusion Long-term administration of Cap and Sar suppressed SHR SMC growth through inhibition of Aug I generation or blockade of Aug I binding to its receptor.