Ambrosioni E, Bacchelli S, Degli Esposti D, Borghi C
Istituto di Patologia Speciale Medica, Lavoro D. Campanacci, Università degli Studi di Bologna, Italy.
Clin Exp Hypertens. 1993;15 Suppl 1:157-72.
The role of renin-angiotensin system in the development of atherosclerosis is not yet defined, even though several actions of angiotensin II have been suggested as contributing to the development of the atherosclerotic lesion. Local renin-angiotensin system may exert a variety of autocrine or paracrine influences on vascular tissue leading to important trophic and growth regulatory effects and participating to well known events in atherogenesis as control of smooth muscle cell growth and proliferation. The existence and the specific function of components of this system in blood vessels wall suggest its possible involvement in atherosclerotic process. On these bases, the antiatherogenic properties of ACE-inhibitors have been recently evaluated in animal models where a protective effect of ACE-inhibition over the development of experimental atherosclerotic lesions has been observed. This favorable effect could follow the antihypertensive action of ACE-inhibitors even whether other potential mechanisms, including prevention of angiotensin II-induced vascular proliferation and interference with sympathetic nervous system activity and insulin sensitivity, have to be considered. Despite some clear-cut experimental evidences, the clinical importance of such findings as well as the precise mechanisms by which ACE-inhibition is able to interfere with the pathogenesis of atherosclerosis is still matter of debate and need to be assessed in future investigations.
尽管已经提出血管紧张素II的几种作用有助于动脉粥样硬化病变的发展，但肾素-血管紧张素系统在动脉粥样硬化发展中的作用尚未明确。局部肾素-血管紧张素系统可能对血管组织产生多种自分泌或旁分泌影响，导致重要的营养和生长调节作用，并参与动脉粥样硬化形成过程中的一些众所周知的事件，如控制平滑肌细胞的生长和增殖。该系统成分在血管壁中的存在及其特定功能表明其可能参与动脉粥样硬化过程。基于这些原因，最近在动物模型中评估了ACE抑制剂的抗动脉粥样硬化特性，在这些模型中观察到ACE抑制对实验性动脉粥样硬化病变的发展具有保护作用。即使必须考虑其他潜在机制，包括预防血管紧张素II诱导的血管增殖以及干扰交感神经系统活动和胰岛素敏感性，这种有利作用也可能是ACE抑制剂的降压作用所致。尽管有一些明确的实验证据，但这些发现的临床重要性以及ACE抑制能够干扰动脉粥样硬化发病机制的确切机制仍存在争议，需要在未来的研究中进行评估。
