Ace-inhibitors and experimental atherosclerosis.

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.