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Angiotensin II (Ang II) exacerbates atherosclerosis in animal models with activated renin-angiotensin systems and hypercholesterolemia.1 Indirect evidence from trials in which angiotensin-converting enzyme inhibitors and Ang II type 1 receptor (AT1R) blockers were efficacious in decreasing cardiovascular events support the notion that Ang II plays a role in the pathogenesis of atherosclerosis clinically.2,3 AT1Rs mediate most of the physiological and pathophysiologic cardiovascular responses to Ang II.4 AT1Rs are involved in the pathophysiology of atherosclerosis.5See page 313 Atherosclerosis is a disease of chronic inflammation of large arteries with intermittent acute exacerbations that are associated with clinical events.6 Leukocytes migrate into the arterial wall after adhering to and migrating through the endothelium. The vascular endothelium normally does not attract adherence of leukocytes or of platelets and, thus, basally is anti-inflammatory and antithrombogenic.6 “Dysfunctional” endothelium, which is associated with the presence of traditional cardiovascular risk factors such as hypercholesterolemia and diabetes mellitus, on the other hand, may attract leukocyte adherence and be prothrombogenic for multiple reasons, including enhanced platelet adherence.6 Dysfunction of the endothelium also is characterized by the loss of its normal role as a vasodilator, a function that is mediated to an important extent by the generation …

Leukocyte and Endothelial Angiotensin II Type 1 Receptors and Microvascular Thrombotic and Inflammatory Responses to Hypercholesterolemia