Abstract

Intravenous administration of dopamine produced a dose-dependent decrease in lower esophageal sphincter pressure and a dose dependent increase in contractile activity of the body of the esophagus. The threshold dose of dopamine was 0.25 mug/kg, and the effect reached a plateau at about 6 mug/kg. A dose of 6 mug/kg of dopamine produced 83%+/-3 (SE) reduction in the lower esophageal sphincter pressure and 12+/-1 (SE) contractions in the body of the esophagus within 5 min of the bolus injection. Atropine, phentolamine, propranolol, and bilateral cervical vagotomy did not modify the effect of dopamine. Both haloperidol and bulbocapnine potently antagonized the effect of dopamine. The amplitude of esophageal contraction in the lower esophagus in response to pharyngeal stimulation and esiogageal distention was significantly increased after administration of haloperidol. It is concluded that intravenous administration of dopamine has potent effects on the motor function of the lower esophageal sphincter and the body of the esophagus. The effect of dopamine is not mediated via the vagal centers in the brain or cholinergic muscarinic and adrenergic receptors. The response of the smooth muscle segment of opossum esophagus to intravenous dopamine is mediated via specific dopamine receptors. The inhibitory dopamine receptors may play a physiological role in controlling the amplitude of esophageal contractions.

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