An α-adrenergic coronary constriction during esophageal distention in the dog

Previous work has shown an increase in sympathetic stimulation of the heart during chemical or mechanical irritation of visceral organs, but the involvement of the coronary circulation in such reflexes is not clear. In five preliminary experiments in anesthetized dogs, esophageal distention produced a sympathetic stimulation of the heart, as evidenced by an increase in heart rate, which was abolished by non-selective β-adrenergic and muscarinic blockades. On the basis of these preliminary data, we further examined a sympathetic coronary constriction during acute esophageal distension in which any direct adrenergic coronary constriction was unmasked by muscarinic blockade with atropine (100 μg/kg. i.v.), and non-selective β-adrenergic blockade with propranolol (1 mg/kg, i.v.). In seven dogs anesthetized with α-chloralose in an open-chest procedure, the esophagus was rapidly distended to a pressure of 36 ± 2 mm Hg. which was not significantly different from the distending pressure used in the preliminary experiments. During esophageal distention, the mean circumflex blood flow decreased to 77 ± 10% (SEM) of the predistention value. This decrease was statistically significant (p < 0.05). There was no change in left ventricular pressure, mean arterial pressure dV/dt_max or heart rate. Intracoronary administration of the nonselective α-adrenergic antagonist phentolamine completely abolished the reduction in mean circumflex coronary blood flow caused by esophageal distention in the presence of β-adrenergic and muscarinic blockades. These results demonstrate a direct sympathetic coronary vasoconstriction elicited by esophageal distention. This vasoconstriction was due to activation of coronary a-adrenergic receptors.