title: 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.
  
  
  METHODS
  Prospective, unblinded, dose-response evaluation in an awake animal.
  
  
  METHODS
  University research laboratory.
  
  
  METHODS
  Thirty newborn piglets, obtained and instrumented at 1 to 3 days of age and studied 48 hrs later.
  
  
  METHODS
  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.
  
  
  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.
authors.affiliation: Perinatal Research Centre, University of Alberta, Edmonton, Canada.
authors.forename: R J
authors.initials: RJ
authors.lastname: Pearson
authors.forename: K J
authors.initials: KJ
authors.lastname: Barrington
authors.forename: D W
authors.initials: DW
authors.lastname: Jirsch
authors.forename: P Y
authors.initials: PY
authors.lastname: Cheung
mesh_terms: D000818:Animals; D000831:Animals, Newborn / Q000502:physiology*; D001783:Blood Flow Velocity / Q000187:drug effects; D004298:Dopamine / Q000494:pharmacology; D018818:Fenoldopam / Q000494:pharmacology; D017538:Mesenteric Artery, Superior / Q000502:physiology; D011446:Prospective Studies; D011954:Receptors, Dopamine / Q000502:physiology*; D012077:Renal Artery / Q000502:physiology; D012079:Renal Circulation / Q000502:physiology*; D013152:Splanchnic Circulation / Q000502:physiology*; D013552:Swine; D014655:Vascular Resistance / Q000187:drug effects; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D011954:Receptors, Dopamine; D014665:Vasodilator Agents; D018818:Fenoldopam; D004298:Dopamine