Coronary vascular responses to nicotine in the anaesthetized dog.

The effect of the intra-coronary (i.c.) injection of nicotine on large coronary artery diameter and coronary blood flow was examined in anaesthetized dogs. In sixteen untreated dogs nicotine (20 micrograms i.c.) had a biphasic effect on arterial pressure (initial increase, 7 +/- 2 mmHg; secondary decrease, -8 +/- 3 mmHg) which was accompanied by small and variable effects on heart rate and an increase in LV dP/dt. Nicotine increased large coronary artery diameter by 5.8 +/- 0.8% but had a biphasic effect on coronary blood flow (initial increase, 41 +/- 7 ml/min; secondary decrease, -10 +/- 2 ml/min). Bilateral vagotomy or muscarinic receptor blockade with atropine (0.1 mg/kg i.v.) did not significantly affect the nicotine-induced changes in coronary artery diameter or coronary blood flow. The additional antagonism of beta-adrenoceptors with propranolol (1 mg/kg i.v.) abolished the effect of nicotine in coronary artery diameter (delta CD = 0.2 +/- 0.2%) and the initial increase in coronary blood flow (delta CBF = 1 +/- 1 ml/min) but enhanced the secondary decrease in flow (delta CBF = -25 +/- 3 ml/min). The nicotine-induced decrease in coronary blood flow observed after muscarinic and beta-adrenoceptor blockade was attenuated by antagonism of alpha 1-adrenoceptors with prazosin (10 micrograms/kg i.c., delta CBF = -15 +/- 3 ml/min) and abolished after additional antagonism of alpha 2-adrenoceptors with idazoxan (50 micrograms/kg i.c., delta CBF = -2 +/- 1 ml/min). These results indicate that in the anaesthetized dog intra-coronary injection of nicotine results in beta-adrenoceptor mediated dilatation of both large and small coronary arteries.(ABSTRACT TRUNCATED AT 250 WORDS)