Objective:To evaluate the effects and possible mechanisms of rutaecarpine on angiotensinⅡ(AngⅡ)-induced proliferation in cultured rat vascular smooth muscle cells(VSMCs).Methods:VSMCs were isolated from Male Sprague-Dawley rat aorta,and cultured by enzymic dispersion method.Experiments were performed with cells from passages 3-8.The cultured VSMCs were randomly divided into control,model(AngⅡ0.1μmol/L),and rutaecarpine(0.3-3.0μmol/L)groups.VMSC proliferation was induced by AngⅢ,and was evaluated by the3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and cell counting.To examine the mechanisms involved in anti-proliferative effects of rutaecarpine,nitric oxide(NO)levels and NO synthetase(NOS)activity were determined.Expressions of VSMC proliferation-related genes including endothelial nitric oxide synthase(eNOS),and c-myc hypertension related gene-1(HRG-1)were determined by real-time reverse transcription-polymerase chain reaction(RT-PCR).Results:Rutaecarpine(0.3-3.0μmol/L)inhibited AngⅡ-induced VSMC proliferation and the best effects were achieved at 3.0μmol/L.The AngⅡ-induced decreases in cellular NO contents and NOS activities were antagonized by rutaecarpine(P<0.05).AngⅡadministration suppressed the expressions of eNOS and HRG-1,while increased c-myc expression(P<0.05).All these effects were attenuated by 3.0μmol/L rutaecarpine(P<0.05).Conclusion:Rutaecarpine is effective against AngⅡ-induced rat VSMC proliferation,and this effect is due,at least in part,to NO production and the modulation of VMSC proliferation-related gene expressions. Objective: To evaluate the effects and possible mechanisms of rutaecarpine on angiotensin II (Ang II) -induced proliferation in cultured rat vascular smooth muscle cells (VSMCs). Methods: VSMCs were isolated from Male Sprague-Dawley rat aorta, and cultured by enzymic dispersion method. Experiments were performed with cells from passages 3-8. The cultured VSMCs were randomly divided into control, model (Ang II 0.1 μmol / L) and rutaecarpine (0.3-3.0 μmol / L) groups. VMSC proliferation was induced by AngⅢ, and was as by the 3- (4,5-dimethylthiazol-2-yl) -2,5-diphenyltetrazolium bromide assay and cell counting. examine the mechanisms involved in anti-proliferative effects of rutaecarpine, nitric oxide (NO) levels and NO synthetase NOS) activity were determined. Expressions of VSMC proliferation-related genes including endothelial nitric oxide synthase (eNOS), and c-myc hypertension related gene- 1 (HRG-1) were determined by real-time reverse transcription- polymerase chain reaction -PCR). Results: Rutaecarpine (0.3-3.0μmol / L) inhibited AngⅡ-induced VSMC proliferation and the best effects were achieved at 3.0μmol / L.The AngⅡ-induced decreases in cellular NO contents and NOS activities were antagonized by rutaecarpine (P <0.05) .AngⅡadministration suppressed The expressions of eNOS and HRG-1, while increased c-myc expression (P <0.05). All these effects were attenuated by 3.0 μmol / L rutaecarpine (P <0.05) .Conclusion: Rutaecarpine is effective against AngⅡ-induced rat VSMC proliferation , and this effect is due, at least in part, to NO production and the modulation of VMSC proliferation-related gene expressions.