Dopaminergic receptor-mediated effects in the mesenteric vasculature and renal vasculature of the chronically instrumented newborn piglet

Abstract

OBJECTIVE: To 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. DESIGN: Prospective, unblinded, dose-response evaluation in an awake animal. SETTING: University research laboratory. SUBJECTS: Thirty newborn piglets, obtained and instrumented at 1 to 3 days of age and studied 48 hrs later. INTERVENTIONS: Animals 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 micrograms/kg/min) or fenoldopam (1 to 100 micrograms/kg/min), which is a selective agonist of the dopamine-1 receptor. MEASUREMENTS AND MAIN RESULTS: Blood pressure was only significantly increased by the highest infusion rate of dopamine (32 micrograms/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 micrograms/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 micrograms/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 micrograms/kg/min. Fenoldopam had no effect on renal vascular resistance at any dose. Fenoldopam reduced mesenteric vascular resistance at 5 micrograms/kg/min and at all higher doses. CONCLUSIONS: These 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.