Abstract
Whether endothelium-derived relaxing factor (EDRF)/nitric oxide (NO) plays a role in the dilation of the left circumflex coronary artery during acute exercise and whether endothelium-mediated dilation of this artery is altered after chronic exercise training have not been determined previously. Nine dogs were chronically instrumented for measurements of systemic hemodynamics, left circumflex coronary artery diameter, and blood flow. Acute treadmill exercise (10.9 km/h) caused dilation of the circumflex coronary artery by 4.33 +/- 0.84% and an increase in coronary blood flow by 32 +/- 5.2 mL/min. After the administration of intravenous nitro-L-arginine, the dilation of the circumflex coronary artery was converted to vasoconstriction (-4.13 +/- 1.58%), whereas the increase in coronary blood flow was not altered (24 +/- 3.6 mL/min). Chronic exercise training (2 hours each day at a speed of 10.9 km/h for 7 days) enhanced acetylcholine-induced dilation and reactive dilation (following release of a brief coronary artery occlusion) of the large coronary artery (P < .05), whereas the coronary blood flow responses were not changed. These enhanced acetylcholine-induced and reactive dilations of the circumflex coronary artery were due to a greater release of EDRF/NO since they were eliminated by nitro-L-arginine. Thus, in the circumflex coronary artery, EDRF/NO-dependent dilation was enhanced after 7 days of exercise training. This may represent the mechanism responsible for the perception that chronic exercise induces cardiovascular "well being."
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