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目的：通过培养的大鼠主动脉内皮细胞，观察ＡｎｇⅡ对ＥＣ分泌ＮＯ，ＥＴ－１的影响及形态学变化和ＮＯ的前体物Ｌ－Ａｒｇ 对ＡｎｇⅡ的抵消作用及对ＥＣ的保护作用。结果：随ＡｎｇⅡ浓度增高ＥＣ生成ＮＯ减低，分泌ＥＴ－１ 增加，加入Ｌ－Ａｒｇ 及卡托普利后ＮＯ生成回升，ＥＴ－１ 分泌减低；高浓度ＡｎｇⅡ及ＬＤＬ胆固醇使ＥＣ释放ＬＤＨ增加，细胞收缩。适量Ｌ－Ａｒｇ 可改善之。结论：高浓度ＡｎｇⅡ，ＥＴ－１ 及ＮＯ生成量减低可能加速ＡＳ及高血压的发生发展
OBJECTIVE: To observe the effects of AngⅡ on the secretion of NO and ET-1 and the morphological changes of Ang Ⅱ and the protective effect of L-Arg on AngⅡ and the protective effect of EC on cultured rat aortic endothelial cells. Results: With the increase of concentration of AngⅡ, the NO production was decreased, the secretion of ET-1 was increased, the production of NO was increased after L-Arg and captopril were added, and ET-1 secretion was decreased. High concentrations of AngⅡand LDL cholesterol increased the release of LDH, shrink. Appropriate amount of L-Arg can be improved. Conclusion: Decreased production of high concentrations of AngⅡ, ET-1 and NO may accelerate the development of hypertension and hypertension