ObjectiveTo determine the effects of stimulation of vascular dopaminergic receptor subtype 1 (dopamine-1) receptors in the renal and mesenteric vascular beds of a neonatal model.DesignProspective, unblinded, dose-response evaluation in an awake animal.SettingUniversity research laboratory.SubjectsThirty newborn piglets, obtained and instrumented at 1 to 3 days of age and studied 48 hrs later.InterventionsAnimals were chronically instrumented with transit time ultrasound flow probes around the left renal and superior mesenteric arteries. They were then intravenously infused with either dopamine (2 to 32 micro gram/kg/min) or fenoldopam (1 to 100 micro gram/kg/min), which is a selective agonist of the dopamine-1 receptor.Measurements and Main ResultsBlood pressure was only significantly increased by the highest infusion rate of dopamine (32 micro gram/kg/min), from a mean of 78 mm Hg at baseline to 87 mm Hg. Mesenteric and renal vascular resistances were unchanged by dopamine at any dose. Dopamine at 32 micro gram/kg/min decreased renal blood flow by 16.6 +/- 19.6 (SD) % and increased renal vascular resistance by 39.6 +/- 41.1% (p < .05). Mesenteric blood flow increased by 15% at 32 micro gram/kg/min (p < .05) but mesenteric vascular resistance was not affected by dopamine. Fenoldopam reduced blood pressure at infusion rates of 5, 10, and 100 micro gram/kg/min. Fenoldopam had no effect on renal vascular resistance at any dose. Fenoldopam reduced mesenteric vascular resistance at 5 micro gram/kg/min and at all higher doses.ConclusionsThese data demonstrate the absence of dopaminergic receptor-mediated vasodilation in the porcine neonatal renal vascular bed. In the mesenteric artery, dopamine-1 receptor-mediated vasodilation may be obtained. Dopamine itself, probably because of stimulation of other receptors, causes renal artery vasoconstriction and does not increase superior mesenteric artery blood flow.(Crit Care Med 1996; 24:1706-1712)