Experimental investigation on the angiotensinIIinduced proliferation and apoptosis in rat vascular smooth muscle celis in vitro

Objective To investigate the proliferation and apoptosis of rat vascular smooth rauscle celis (VSMCs)in-duced by angiotensin Ⅱ (Ang Ⅱ )and its mechanism. Methods Cultured VSMCs were obtained from rat throacix aorta. Proliferation and apoptosis were deterrnined by cell count and/or Flow cytometer (FCM) . Results (1) Ang Ⅱ can stinulate the proliferation of VSMCs significantly and the eflfect is concentration dependent until it reachs 10 μmol/L. Ang Ⅱ can promote VSMCs entering S phase from G0/G1 phase and DNA synthesis. (2) Both losartan and CGP42112A can cancel the stimulating effect of AngⅡ on VSMCs proliferation. (3) 100μmol/L Angli can induce the apoptosis of VSMCs, and the effect is amplified by prolonged time. CGP42112A can cancel the apoptosis of VSMCs induced by Ang Ⅱ , but losartan can not. Conclusion Results show that Angli can promote the DNA synthe-sis and proliferation of VSMCs both through AT-1 receptor and AT-2 receptor, and Angli can also induce the apoptosis of VSMCs, which may be mostly activated through AT-2 receptor.