Reflex epicardial coronary vasoconstriction elicited by nicotine in anaesthetized dogs.

The effects of arterial chemoreceptor activation by nicotine on coronary artery diameter was studied in anaesthetized, artificially ventilated dogs. Left circumflex coronary artery diameter, coronary blood flow, calculated mean coronary resistance, systemic arterial blood pressure and heart rate were measured. In control dogs (n = 10) the injection of nicotine (100 micrograms) into the carotid artery evoked an increase of arterial pressure (+22 +/- 9 mm Hg) and a decrease in heart rate (-36 +/- 13 beats/min), and tended to increase coronary blood flow (+7 +/- 4 ml/min). Intracarotid nicotine had no effect on large coronary artery diameter (+0.02 +/- 0.03 mm) or total coronary resistance (+0.04 +/- 0.09 mm Hg min/ml) under these conditions. When heart rate was controlled by (1) beta-adrenoceptor blockade (propranolol, 1 mg/kg i.v.) plus pacing of the right ventricle (n = 4) or (2) beta-adrenoceptor blockade plus bilateral vagotomy (n = 7), the chemoreflex-induced constriction of the large coronary artery (-0.07 +/- 0.02 mm and -0.12 +/- 0.03 mm, respectively; p less than 0.05). In contrast, there was no chemoreflex-induced change in total coronary resistance after beta-adrenoceptor blockade plus pacing (+0.01 +/- 0.09 mm Hg min/ml, but after beta-adrenoceptor blockade plus vagotomy coronary resistance was increased (+0.75 +/- 0.31 mm Hg min/ml; p less than 0.05). The constriction of both large and small coronary arteries was abolished by phentolamine (0.5 mg/kg i.v.). These results suggest that carotid body chemoreceptor stimulation by nicotine can produce reflex alpha-adrenoceptor-mediated constriction of both large and small coronary arteries, and that the constriction of the small vessels is balanced by vagally-mediated dilatation.