Vasoconstrictor actions of atrial natriuretic peptide in the splanchnic circulation of anesthetized dogs

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Intravenous atrial natriuretic peptide (ANP) usually results in splanchnic vasoconstriction in humans or experimental animals that is accompanied by falls in blood pressure and/or cardiac output. To determine direct in vivo effects in the present study, ANP was infused (12 ng-kg-1·min-1) directly into the mesenteric (iMA) and hepatic (iHA) arterial beds of anesthetized dogs, thereby minimizing changes in blood pressure. Over the first 2 min of iMA infusion, rate of change in mesenteric vascular resistance was 19.6 ± 5.4 mmHg·1-1·min-1/min, reaching a maximum increase in resistance of 22 ± 4% compared with baseline after ~10 min. There was no evidence of vasodilatation at any stage. The mesenteric response was similar whether ANP was infused iMA, iHA, or via the femoral vein (30 ng- kg-1·min-1). In contrast, hepatic vasoconstrictor response to ANP infusion ilia or into the portal vein was only evident after ~5 min, reaching a maximum increase in hepatic vascular resistance of 11 z 6% after ~15 min ilia infusion. When preinfused through the gut vasculature (iMA), ANP increased hepatic vascular resistance earlier and reached similar levels (14 ± 3%), despite a lower arterial concentration of ANP. It is proposed that a vasoconstrictor agent from the intestinal circulation contributed to ANP-induced splanchnic vasoconstriction.

Original languageEnglish
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Issue number6 44-6
Publication statusPublished - 1998
Externally publishedYes


  • Atrial natriuretic factor
  • Blood flow
  • Fractional extraction
  • Hepatic artery
  • Hepatic autoregulation
  • In vivo
  • Intestinal tract
  • Mesenteric artery
  • Vascular resistance
  • Vasoconstriction

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