肾素-血管紧张素系统与静脉移植术后内膜增生的研究进展

Progress in the study of the relationship between the renin angiotensin system and the intimal hyperplasia after vein transplantation

血管内膜增生导致的再狭窄降低了血管的通畅率,限制了自体静脉移植术、冠脉旁路移植术等心血管手术的成功率。内膜增生的关键因素是血管平滑肌细胞(vascular smooth muscle cell,VSMC)的异常增殖、迁移及细胞外基质(extra cellular matrix,ECM)在内膜的沉积。肾素-血管紧张素系统(renin angiotensin system,RAS)参与VSMC的增殖、迁移及内皮功能的调节,在减轻血管内膜增生中有一定的作用。RAS中的血管紧张素Ⅱ(angiotensinⅡ,AngⅡ)与AT1R结合后可促进VSMC的增殖、迁移,与AT2R结合后可产生拮抗AT1R的生理效应。血管紧张素(1-7)〔angiotensin(1-7),Ang(1-7)〕可与Mas结合发挥与激活AT2R相似的效应,AngⅡ可能是内膜增生的潜在调控者。血管紧张素转化酶抑制剂(angiotensin converting enzyme inhibitor,ACEI)和血管紧张素受体阻滞剂(angiotensin receptor blocker,ARB)有可能作为减轻内膜增生的药物,提高血管移植的通畅率。

Restenosis caused by vascular intimal hyperplasia reduces vascular patency rate and limits the success rate of cardiovascular surgery such as autologous vein graft, coronary artery bypass grafting, and so on. Key factors of intimal hyperplasia is the abnormal proliferation and migrationof vascular smooth muscle cell （VSMC） and the extracellular matrix （ECM） deposition in the endometrium. Renin angiotensin system （RAS） which involves in the proliferation and migration of VSMC, as well as the regulation of endothelial function, plays an important role in reducing intimal hyperplasia. Ang Ⅱ combined with AT1R can promote the proliferation and migration of VSMC, Ang Ⅱ combined with AT2R have antagonistic effects on the physiological effects of AT1R. Ang （1-7） can be combined with Mas to play a similar effect with activation AT2R. Ang Ⅱ may be a potential regulator of intimal hyperplasia. Angiotensin converting enzyme inhibitors （ACEI） and angiotensin receptor blocker （ARB） may be used as a drug to reduce intimal hyperplasia and improve the patency rate of vascular graft.