Characterization of Vascular Dopamine Receptors in the Gastric Circulation of the Rabbit

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Abstract
An in vivo model is presented for studying the vasodilator effect of dopamine on the gastric vascular bed of the anesthetized rabbit. Dopamine was injected into the common hepatic artery simultaneously measuring the blood flow through the left gastric artery at constant perfusion pressure. The vasoconstrictor response to dopamine was blocked by pretreatment with phenoxybenzamine (0.5 mg/kg i.a.). Dopamine dilated the gastric vascular bed dose-dependently with an average ED50 of 15 nmol. Apomorphine caused vasodilation with an ED50 of 38.8 nmol; the maximum response was significantly lower than with dopamine. (-)Isoproterenol was ineffective. cis-Flupentixol (3.5 and 7.0 .mu.mol/kg i.v.) and (+)butaclamol (3.0 .mu.mol/kg i.v.), but not trans-flupentixol (7.0 .mu.mol/kg i.v.) and (-)butaclamol (6.0 .mu.mol/kg i.v.) shifted the dopamine dose-response curve to the right in a parallel fashion, indicating competitive antagonism. Haloperidol, bulbocapnine, and sulpiride also acted as competitive inhibitors of dopamine-induced vasodilation. The antagonists inhibited the dopamine-induced vasodilation in the following order of potency: (+)butaclamol > cis-flupentixol > haloperidol > bulbocapnine > sulpiride. The results suggest that the vascular dopamine receptors in the stomach of the rabbit resemble the DA1-receptors in the mesenteric vascular bed of dogs.