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目的观察阿托伐他汀钙对AngⅡ诱导的人脐静脉内皮细胞（human umbilical vein endothelial cells，HUVECs）表达诱导型一氧化氮合酶（inducible nitric oxide synthase，iNOS）及一氧化氮（nitric oxide，NO）生成的影响，讨论二者之间的关系和可能机制。方法体外培养HUVECs，用102030阿托伐他汀钙预处理HUVECs 24 h，再与10-7 mol/L AngⅡ共同孵育12 h；通过RT-PCR和Western Blot分别检测iNOS mRNA和蛋白表达水平；通过Griees反应测定上清NO释放量。结果与无刺激组比较，10-7 mol/L AngⅡ刺激HUVECs 12 h后明显上调iNOS mRNA及蛋白表达，<0.001；基础状态下HUVECs不表达iNOS（无论mRNA还是蛋白），10-7 mol/L AngⅡ刺激8 h后明显增加iNOS mRNA和蛋白表达（与对照组相比，<0.001）；不同浓度（10、20、30μmol/L）阿托伐他汀钙预处理24 h明显抑制AngⅡ对HUVECs iNOS mRNA及其蛋白表达的上调作用（与AngⅡ组相比，0.05，无统计学意义）。与无刺激组比较10-7 mol/L AngⅡ明显减少NO的释放，<0.001，有统计学意义；与AngⅡ组比较，阿托伐他汀钙干预24 h后呈浓度趋势增加NO的释放，<0.001，有统计学意义。结论阿托伐他汀钙呈浓度效应抑制AngⅡ诱导的HUVECs表达iNOS，并呈浓度趋势增加内皮NO的释放。“,”Objective 3-hydroxy-3-methylglutaryl-coenzyme a (HMG-CoA)reductase inhibitors (atorvastatin)reduce lesion formation in animal models of atherosclerosis by mechanisms that have not been defined completely. We hypothesized that atorvastatin inhabit the expression of inducible nitric oxide release (iNOS)stimulated by AngII to protect the vascular wall which may be related to the enhancement on expression of endothelial nitric oxide synthase(eNOS).Methods Human umbilical vein was isolated and culcured passage 3~5 of cultured HUVECs were preincubated for 24 h with Cig (0.1 mol/L,1 mol/L,10 mol/L,100 mol/L),then incubated with10-7mol/L AngIIfor 12 h. Total RNA was extracted,and eNOS expression both mRNA and protein was assessed by RT-PCR and Western Blot. NO production was measured via griess reaction. Results Atorvastatin markedly enhanced the expression of AngII- induced iNOS ( <0.01, <0.001),both mRNA and protein level,and stimulated NO release from human umbilical vein endothelial cells activated by AngiotensinII (0.1M ,atorvastatin 10M ,20M ,30M P<0.001). Conclusion Taken together,these findings demonstrate that atorvastatin could decreased the expression of iNOS induced by AngII,and stimulated NO release from HUVECs,which maybe correlate to a transcriptional mechanism of eNOS expression.