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肾素血管紧张素系统（RASS）的效应分子为血管紧张素Ⅱ(AngⅡ)，对内皮细胞及平滑肌细胞的功能具有重要的影响。血管紧张素II不仅影响血流动力学效应，还通过其血管紧张素1 受体（AT1R）发挥强大的促氧化和促炎症反应的效应。在内皮细胞和白细胞中血管紧张素Ⅱ通过烟酰胺腺嘌呤二核苷酸磷酸盐（NADPH）氧化酶的激活和细胞内氧化还远信号传导系统从而促进脉管系统炎症反应的形成，血管紧张素Ⅱ和葡萄糖在内皮细胞和炎性细胞中还共享氧化还原信号传导通路，可见血管紧张素Ⅱ参与了炎症的反应、血栓的形成，通过刺激细胞因子和生长因子进行细胞的增值，血管紧张素Ⅱ的这些效应与胰岛素抵抗、氧化应激以及血管内皮细胞的损伤有着密切的联系，并且有研究显示应用RASS 抑制剂可以有效地延缓心脑血管疾病的进展，这些证据显示抑制RASS 系统在保护血管病变的重要性。

英文摘要:

Angiotensin II, the effector molecule of the renin-angiotensin system, has profound effects on endothelial and smooth muscle cells. These effects are not only hemodynamic in nature, but also angiotensin II has considerable pro-oxidant and proinflammatory effects by binding to its type 1 receptor angiotensinII activates NADPH oxidase and induces redox signalling in both endothelial cells as well as leucocytes. Angiotensin II stimulates the formation of proinflammatory cytokines from the vasculature, Angiotensin II and glucose share components of their intracellular redox signaling pathways in endothelial and inflammatory cells. Thus can be seen angiotensin II Participated in the comprise inflammation, thrombosis, and cell proliferation through stimulation of production of cytokines and growth factors, angiotensin II of these effects associated with insulin resistance, oxidative stress and endothelial cell injury are closely linked, and the application of RASS inhibitor can effectively slow the progression of cardiovascular and cerebrovascular diseases, suggestive evidence for this notion is the impressive beneficial effect of pharmacological interference with the renin-angiotensin systemin large vessel disease.

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