Contraction of bovine coronary vascular smooth muscle induced by cocaine is not mediated by norepinephrine.

This study was designed to assess the effects of cocaine on coronary arterial smooth muscle and to determine whether previously reported cocaine-induced coronary vasospasm is mediated by substances released from the endothelium or by increased adrenergic receptor stimulation. Concentration-response relationships for cocaine (0.1-300 microM) and norepinephrine (0.1-300 microM) were studied in vitro using 2 mm segments of bovine proximal left anterior descending coronary artery. Each segmental ring was mounted in a 70 ml tissue bath for the measurement of isometric tension. Cocaine (3-300 microM) caused significant, concentration-dependent, increases in developed tension (p less than 0.05). Removal of the endothelium or pretreatment with prazosin (0.1 microM) or propranolol (1 microM) did not significantly alter this action of cocaine. In contrast to cocaine, norepinephrine (10-300 microM) caused significant decreases in developed tension (p less than 0.01). These findings suggest that cocaine-induced contraction of bovine coronary vascular smooth muscle is not mediated by endothelium derived contracting substances or norepinephrine.