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 …
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