Stajszczyk M, Gmiński J
Katedra i Zakład Biochemii i Chemii Slaskiej Akademii Medycznej w Katowicach.
Postepy Hig Med Dosw. 1996;50(6):635-47.
Blockade of the renin-angiotensin system reduces the development of the atherosclerotic process after vascular injury and in hyperlipidemic animals. ACE-inhibitors inhibit vascular smooth muscle cells migration and proliferation, macrophage-foam cell accumulation and preserve the antiaggregatory and antithrombotic function of the endothelium in atherosclerotic vessels. In addition to the inhibition of angiotensin II synthesis, reduced degradation of kinins and improvement of insulin action after ACE-inhibition may be responsible for observed actions. ACE-inhibitors may have also influence on lipids metabolism, including low density lipoprotein oxidation. Despite this, ACE-inhibitors failed to prevent restenosis after coronary angioplasty in humans. One reason for the lack of ACE-inhibitors effect in human restenosis might depend on the activation of the alternative angiotensin II-generating system in human arteries after vascular injury.
阻断肾素-血管紧张素系统可减少血管损伤后及高脂血症动物动脉粥样硬化进程的发展。血管紧张素转换酶抑制剂（ACE抑制剂）可抑制血管平滑肌细胞迁移和增殖、巨噬细胞-泡沫细胞积聚，并维持动脉粥样硬化血管内皮的抗聚集和抗血栓形成功能。除了抑制血管紧张素II的合成外，ACE抑制后激肽降解减少和胰岛素作用改善可能是其观察到的作用的原因。ACE抑制剂也可能影响脂质代谢，包括低密度脂蛋白氧化。尽管如此，ACE抑制剂未能预防人类冠状动脉成形术后的再狭窄。ACE抑制剂在人类再狭窄中缺乏作用的一个原因可能取决于血管损伤后人类动脉中替代血管紧张素II生成系统的激活。
