PURPOSE OF REVIEW - While it is well established that angiotensin II promotes cardiovascular and renal disorders, recent evidence has indicated a pivotal role in atherosclerotic disease which is distinguished by the central abnormality of lipid accumulation within the vascular wall.
RECENT FINDINGS - Studies published in the last year show that angiotensin II activity is increased in atherosclerosis, but even a transient elevation in angiotensin II potentiates the disease. The downstream hormone, aldosterone, has vasculopathic effects in conjunction with, as well as independently of, angiotensin II. The mechanism for angiotensin II injury includes potentiation of damage by known risk factors such as hypertension, hyperlipidemia, diabetes and insulin resistance, falling estrogens and inflammation. In addition, angiotensin II has direct effects on cellular proliferation, hypertrophy, apoptosis, and synthesis/degradation of matrix proteins and collagen that underlie development and progression of atherosclerosis as well as stability of the plaque. Antagonism of angiotensin II actions, therefore, offers the possibility of interfering with these direct and indirect effects and lessening the progression of atherosclerosis, stabilizing vulnerable plaques, and even reversing the disease.
SUMMARY - Angiotensin is increased in atherosclerosis, and increased angiotensin II amplifies atherosclerosis by modulating individual risk factors as well as by directly affecting lipid metabolism, the vascular response to lipid accumulation, and plaque stability. Antagonism of angiotensin II actions not only lessens the progression of atherosclerosis, but stabilizes the plaque and may even cause regression of the disease.