Action of nicotine on coronary vascular resistance in dogs.

The effect of nicotine, norepinephrine, acetylcholine, and sympathetic and parasympathetic nerve stimulation on perfusion pressure in the left descending coronary artery has been evaluated. Nicotine administered intra-arterially produced an increase in coronary vascular resistance as indicated by an increase in coronary perfusion pressure. It was concluded that this results from sympathetic nervous system activity or release of catecholamines from chromaffin tissue. Ganglia or ganglion-like structures are apparently involved. Other drugs and procedures that were used in attempting to localize the site of nicotine action are discussed. The experimental procedures were also used with preparations that measured myocardial force of contraction. The contractile force of the myocardium, as well as coronary perfusion pressure, was increased with intracoronary administration of nicotine or norepinephrine and sympathetic nerve stimulation. Coronary vascular resistance was increased by these agents and procedures. Vagal nerve stimulation or intracoronary administration of acetylcholine usually decreased the force of contraction and coronary perfusion pressure.