Modulation of coronary autoregulatory responses by nitric oxide: Evidence for flow-dependent resistance adjustments in conscious dogs

Abstract

The present study tested the hypothesis that nitric oxide production in coronary resistance vessels is an important mechanism affecting the regulation of myocardial perfusion in unanesthetized dogs. We inhibited nitric oxide synthesis with the arginine analogue Nω-nitro-L-arginine methyl ester (L-NAME, 10 mg/kg) and maintained the compressive determinants of myocardial blood flow constant by ventricular pacing. L-NAME did not affect resting coronary blood flow and reduced the receptor-mediated increase in flow to intracoronary acetylcholine (100 μg/min IC) from 143±20% (mean±SEM) under control conditions to 31±10% after L-NAME (P