Numerous clinical and laboratory data are now available supporting the hypo
thesis that the renin-angiotensin system is mechanistically relevant in the
pathogenesis of atherosclerosis. The traditional role of the renin-angiote
nsin system in the context of blood pressure regulation has been modified t
o incorporate the concept that angiotensin II (Ang II) is a potent proinfla
mmatory agent. In vascular cells, Ang II is a potent stimulus for the gener
ation of reactive oxygen species. As a result, Ang II upregulates the expre
ssion of many redox-sensitive cytokines, chemokines, and growth factors tha
t have been implicated in the pathogenesis of atherosclerosis. Extensive da
ta now confirm that inhibition of the renin-angiotensin system inhibits ath
erosclerosis in animal models as well as in humans. These studies provide m
echanistic insights into the precise role of Ang II in atherosclerosis and
suggest that pharmacologic interventions involving the renin-angiotensin sy
stem may be of fundamental importance in the treatment and prevention of at
herosclerosis. (C) 2001 by Excerpta Medica, Inc.