Endothelium-derived nitric oxide does not modulate metabolic coronary vasodilation induced by tachycardia in dogs.

Endothelium-derived nitric oxide (EDNO) has been implicated in the modulation of coronary arterial tone. The aim of this study was to determine if metabolic coronary vasodilation induced by pacing tachycardia is altered by the inhibition of EDNO synthesis. Before and after the intracoronary infusion of an inhibitor of EDNO synthesis (N omega-nitro-L-arginine-methyl-ester, L-NAME), changes in coronary blood flow (CBF), regional myocardial blood flow (MBF), and myocardial oxygen consumption (MVO2) were measured in anesthetized dogs in response to atrial pacing tachycardia. Increasing the heart rate from 109 +/- 10 to 160 beats/min by pacing produced significant increases in CBF (p < 0.05), MVO2 (p < 0.05), and MBF in each sublayer of the myocardium (p < 0.05). L-NAME did not alter the pacing-induced increases in CBF, MVO2, or regional MBF. In addition, the ratio of the tachycardia-induced increase in CBF to the increase in MVO2 was not changed by L-NAME. The coronary vasodilation evoked by acetylcholine was attenuated by L-NAME (p < 0.05). However, the response to sodium nitroprusside was not altered. These results suggest that EDNO does not play a primary role in the mechanism mediating metabolic coronary vasodilation induced by pacing tachycardia in dogs.