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Ace-inhibitors and experimental atherosclerosis
E Ambrosioni1, S Bacchelli, D Degli Esposti
1Istituto di Patologia Speciale Medica, Lavoro D. Campanacci, Università degli Studi di Bologna, Italy.
Abstract:
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.
Insights
The renin-angiotensin system
Area of Science:
- Cardiovascular Science
- Vascular Biology
- Pharmacology
Background:
- The renin-angiotensin system's role in atherosclerosis is unclear, though angiotensin II may promote lesion development.
- Local renin-angiotensin system components in blood vessels suggest involvement in atherogenesis.
- Angiotensin II influences vascular cell growth and proliferation, key events in atherosclerosis.
Purpose of the Study:
- To evaluate the antiatherogenic potential of angiotensin-converting enzyme (ACE) inhibitors.
- To investigate the mechanisms by which ACE inhibition may affect atherosclerosis.
Main Methods:
- Evaluation of ACE-inhibitor effects in animal models of experimental atherosclerosis.
- Assessment of ACE-inhibitor impact on vascular smooth muscle cell proliferation.
- Consideration of antihypertensive and other potential mechanisms of ACE inhibition.
Main Results:
- ACE-inhibitors demonstrated a protective effect against experimental atherosclerotic lesion development in animal models.
- ACE-inhibition may prevent angiotensin II-induced vascular proliferation.
- Potential interference with sympathetic nervous system activity and insulin sensitivity was noted.
Conclusions:
- ACE-inhibitors show promise in preventing atherosclerosis development, as evidenced in animal studies.
- Further clinical investigations are needed to confirm the clinical significance and elucidate precise mechanisms of ACE-inhibition in atherosclerosis pathogenesis.