Angiotensin II and atherosclerosis

Numerous clinical and laboratory data are now available supporting the hypothesis that the renin–angiotensin system is mechanistically relevant in the pathogenesis of atherosclerosis. The traditional role of the renin–angiotensin system in the context of blood pressure regulation has been modified to incorporate the concept that angiotensin II (Ang II) is a potent proinflammatory agent. In vascular cells, Ang II is a potent stimulus for the generation of reactive oxygen species. As a result, Ang II upregulates the expression of many redox-sensitive cytokines, chemokines, and growth factors that have been implicated in the pathogenesis of atherosclerosis. Extensive data now confirm that inhibition of the renin–angiotensin system inhibits atherosclerosis in animal models as well as in humans. These studies provide mechanistic insights into the precise role of Ang II in atherosclerosis and suggest that pharmacologic interventions involving the renin–angiotensin system may be of fundamental importance in the treatment and prevention of atherosclerosis.