Nitric oxide and coronary endothelial dysfunction in humans.
نویسنده
چکیده
1. Introduction composed of two divergent actions, that is, vasodilation by the stimulated release of NO and other vasodilating The endothelium provides a variety of important func-substances such as EDHF from the endothelium, and direct tions involved in the cardiovascular homeostasis. The vasoconstricting effects on the underlying vascular smooth assessment of endothelial function in humans has focused muscle, particularly with higher doses. In contrast to primarily on endothelial dependent vasomotion in response acetylcholine, bradykinin—and possibly substance P—is to the release of NO. In particular, clinical studies have likely to play a physiological role. Tissue bradykinin is evaluated vasomotor tone following changes in flow or inactivated by the endothelial angiotensin-converting en-stimuli for the release of NO from the endothelium, such zyme [6] and can be released by increased flow [7]. as acetylcholine, substance P or serotonin [1]. However, Endogenous bradykinin appears to be involved in the NO not only acts as a vasodilating substance but also regulation of basal and flow-mediated coronary vasomotor affects other functions of the endothelium such as the tone in humans [8]. However the vasodilator effect of adhesive properties of the endothelium with respect to the bradykinin involves not only NO but also PGI and EDHF.
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ورودعنوان ژورنال:
- Cardiovascular research
دوره 43 3 شماره
صفحات -
تاریخ انتشار 1999