Abstract
The endothelium plays a key role in the regulation of vasoreactivity. To assess its importance on coronary flow regulation, we studied the participation of endothelium-derived relaxing factor-nitric oxide (EDRF-NO) on coronary reactive hyperemia and on the hyperemia that occurs secondary to an increase in myocardial oxygen consumption. In 15 dogs, the reactive hyperemic response decreased substantially after inhibition of EDRF-NO synthesis with N-ω-nitro-L-arginine (P<0.01). In contrast, the hyperemia secondary to an increase in myocardial oxygen consumption, characterized by a linear correlation between myocardial oxygen consumption and coronary flow, did not change significantly after inhibition of EDRF-NO production (regression analysis, P>0.1). Thus EDRF-NO synthesis by the endothelium is an important mechanism mediating the reactive hyperemic response but it does not seem to be essential for the metabolic regulation of coronary vascular resistance during hyperemia induced by an increased metabolic demand on the myocardium.
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