Role of EDRF/NO in parasympathetic coronary vasodilation following carotid chemoreflex activation in conscious dogs

The role of endothelium-derived relaxing factor (EDRF) in parasympathetic coronary vasodilation following carotid chemoreflex activation induced by nicotine in conscious dogs and stimulation of the vagus nerve in anesthetized dogs was studied. Injection of nicotine (11 +/- 4 micrograms) into the carotid artery increased coronary blood flow (CBF) by 126 +/- 16% from 28 +/- 3 ml/min and reduced late diastolic coronary resistance (LDCR) by 43 +/- 4% from 3.58 +/- 0.52 mmHg.ml-1.min, accompanied by a significant increase in mean arterial pressure and a decrease in heart rate (all P < 0.01). Pacing and propranolol did not change the coronary vascular response to chemoreflex activation. There were still increases in CBF by 113 +/- 17% from 29 +/- 3 ml/min and decreases in LDCR by 41 +/- 5% from 3.13 +/- 0.52 mmHg.ml-1.min (all P < 0.01). After infusion of N omega-nitro-L-arginine (L-NNA) (30 mg/kg), the increase in CBF following chemoreflex activation was only 23 +/- 3% from 37 +/- 3 ml/min, and the fall in LDCR was 19 +/- 3% from 3.09 +/- 0.51 mmHg.ml-1.min. Stimulation of the vagus nerve showed a relationship between stimulation frequency and coronary vasodilation that was significantly inhibited by L-NNA. Thus EDRF plays an important role in mediating parasympathetic coronary vasodilation during chemoreflex activation and perhaps during many reflexes that cause vagal cholinergic vasodilation in the heart.