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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2008;28:4.)
© 2008 American Heart Association, Inc.

Editorials

Angiotensin II and New Vessel Formation

Aiming for the Right Oxidative Window

Juan C. Velasquez-Castano; W. Robert Taylor

From the Department of Medicine, Division of Cardiology, Emory University School of Medicine and the Atlanta V.A. Medical Center, Atlanta, Ga.

Correspondence to W. Robert Taylor, MD, PhD, Cardiology Division, Emory University School of Medicine, 1639 Pierce Drive, Suite 319 WMB, Atlanta, GA 30322. E-mail wtaylor@emory.edu

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

New vessel formation is a critical component of homeostatic adaptation to ischemia and infarction. Well-developed collateral circulation confers a better prognosis in patients with acute myocardial infarction and stable coronary artery disease.^1,2 However, approaches used to manipulate vessel growth in animal models have had limited success when translated into new therapies for patients with cardiovascular disease.

See page 61

As an agonist of the NADPH oxidase, angiotensin II (Ang II) has long been recognized as a prooxidant, a feature that is central to its role as a proinflammatory agent in cardiovascular pathophysiology.³ Like other proinflammatory stimuli,⁴ Ang II has been reported to have an almost paradoxical effect in inducing new vessel formation. The growth-stimulatory effects of Ang II on the vasculature are well documented and potentially entirely consistent with a positive effect on new vessel formation. However, the ultimate effect of Ang II on new vessel formation is controversial as it has been reported to both stimulate and inhibit vessel growth.⁵ One possible explanation for these conflicting data includes the differences in the pharmacokinetic and pharmacodynamic profiles of the various therapeutic agents that have been tested. Specifically, tissue affinity has been proposed to influence the potential role that angiotensin converting enzyme (ACE) inhibitors play in regulating the formation of new vessels. Those with high tissue affinity appear to be more likely to promote vascularization.⁶ Other potential mitigating factors include Ang II regulation of vascular endothelial growth factor expression and the effects of ACE inhibition on bradykinin levels. In the latter . . . [Full Text of this Article]

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The Mechanistic Basis for the Disparate Effects of Angiotensin II on Coronary Collateral Growth

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Arterioscler Thromb Vasc Biol 2008 28: 61-67. [Abstract] [Full Text] [PDF]