Published online before print February 19, 2007, doi: 10.1161/01.HYP.0000259601.38807.a6
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(Hypertension. 2007;49:748.)
© 2007 American Heart Association, Inc.
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Methods for Evaluating Endothelial Function in Humans
From the Cardiovascular Research Institute, Washington Hospital Center, Washington, DC.
Correspondence to Julio A. Panza, Coronary Care Unit, Washington Hospital Center, 110 Irving St, NW, Suite 2A74, Washington, DC 20010. E-mail julio.a.panza@medstar.net
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
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Introduction |
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The endothelium is the main regulator of vascular wall homeostasis. Physiologically, endothelial cells maintain a relaxed vascular tone and low levels of oxidative stress, in part by releasing mediators, including NO, prostacyclin (PGI2), and endothelin (ET-1), and controlling local angiotensin II activity.1 In addition, the endothelium actively regulates vascular permeability to plasma constituents, platelet and leukocyte adhesion and aggregation, and thrombosis.1 This state of balanced endothelial regulation of blood vessel function is, however, altered by a number of conditions. Thus, in response to a variety of noxious stimuli, the endothelium undergoes a phenotypic modulation to a nonadaptive state, commonly termed "endothelial dysfunction," characterized by loss or dysregulation of homeostatic mechanisms operative in healthy endothelial cells. This pathophysiological condition is associated with increased expression of adhesion molecules, increased synthesis of proinflammatory and prothrombotic factors, increased oxidative stress, and abnormal modulation of vascular tone, which may lead to different functional manifestations, including impaired endothelium-dependent vasodilation.2
Current evidence suggests that endothelial dysfunction occurs early in the process of atherogenesis and contributes to the formation, progression, and complications of the atherosclerotic plaque.3 Several studies from our and other laboratories have shown that patients with cardiovascular risk factors but no clinical evidence of atherosclerosis have endothelial dysfunction, indicated by an impaired response to endothelial vasodilator agents, such as acetylcholine and bradykinin.4 Combined with the pathophysiological role of the endothelium described above, these observations strongly suggest that endothelial dysfunction is a common mechanistic link between risk factors and the development of atherosclerosis. Furthermore, recent reports
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