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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2006;26:240.)
© 2006 American Heart Association, Inc.

Editorials

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

R. Wayne Alexander

From the Department of Medicine, Emory University School of Medicine, Atlanta, Ga.

Correspondence to R. Wayne Alexander, Chair, Department of Medicine, Emory University School of Medicine, 1364 Clifton Rd NE, EUH H-153, Atlanta, GA 30322. E-mail ralexan@emory.edu

An extract of the first 250 words of the full text is provided, because this article has no abstract.

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.⁵

See 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 of NO by endothelial NO synthase.⁷ In dysfunctional endothelium, NO is degraded by reactive oxygen species (ROS) from several sources, including prominently NADPH oxidases activated by Ang II through the AT1R⁸ and by hyperlipidemia and insulin resistance and hyperglycemia.⁹

Formation of atherosclerotic lesions is a characteristic consequence of endothelial dysfunction in large arteries. . . . [Full Text of this Article]

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Role of Blood Cell–Associated AT1 Receptors in the Microvascular Responses to Hypercholesterolemia

Thomas Petnehazy, Karen Y. Stokes, Katherine C. Wood, Janice Russell, and D. Neil Granger
Arterioscler Thromb Vasc Biol 2006 26: 313-318. [Abstract] [Full Text] [PDF]

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