ENDOTHELIUM-DERIVED NITRIC-OXIDE DOES NOT MODULATE METABOLIC CORONARYVASODILATION INDUCED BY TACHYCARDIA IN DOGS

Endothelium-derived nitric oxide (EDNO) has been implicated in the mod ulation of coronary arterial tone. The aim of this study was to determ ine if metabolic coronary vasodilation induced by pacing tachycardia i s altered by the inhibition of EDNO synthesis. Before and after the in tracoronary 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 consumpt ion (MVo(2)) were measured in anesthetized dogs in response to atrial pacing tachycardia. Increasing the heart rate from 109 +/- 10 to 160 b eats/min by pacing produced significant increases in CBF (p < 0.05), M Vo(2) (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, MVo(2), o r regional MBF. In addition, the ratio of the tachycardia-induced incr ease in CBF to the increase in MVo(2) was not changed by L-NAME. The c oronary vasodilation evoked by acetylcholine was attenuated by L-NAME (p < 0.05). However, the response to sodium nitroprusside was not alte red. These results suggest that EDNO does not play a primary role in t he mechanism mediating metabolic coronary vasodilation induced by paci ng tachycardia in dogs.