Original Article Heart, Circulation, Respiration and Blood; Environmental and Exercise Physiology

Pflügers Archiv

, Volume 429, Issue 3, pp 301-305

First online:

Nitric oxide mediates intestinal hyperaemic responses to intraluminal bile-oleate

  • Wieslaw W. PawlikAffiliated withInstitute of Physiology, University School of Medicine
  • , Piotr GustawAffiliated withInstitute of Physiology, University School of Medicine
  • , Eugene D. JacobsonAffiliated withWebb-Waring Institute for Biomedical Research, University of Colorado Health Sciences Center
  • , Ryszard SendurAffiliated withInstitute of Physiology, University School of Medicine
  • , Krzysztof CzarnobilskiAffiliated withInstitute of Physiology, University School of Medicine

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It has long been recognized that intestinal blood flow increases at mealtimes. Mesenteric hyperaemia is also evoked by activation of sensory peptidergic nerves. Our studies explored the possible role of endogenous nitric oxide (NO) in the rat intestinal vasodilator response to luminal instillation of an oleic acid plus bile mixture before and after acute intrajejunal instillation of capsaicin and after chronic pretreatment with capsaicin. In anaesthetized rats we measured jejunal blood flow (BF) with an ultrasonic Doppler flowmeter and systemic arterial pressure (AP) with a pressure transducer. Intestinal perfusion with 80 mM oleic acid in bile increased BF by 98±12%. Instillation of 4 mg of capsaicin into the jejunal lumen initially increased BF by 42±9% but was followed by vasoconstriction. Inhibition of NO synthase with 25 mg/kg i.v. N-nitro-L-arginine (L-NNA) decreased BF by 27±5% and increased AP by 37±11%. After treatment with L-NNA and after acute and chronic administration of capsaicin, the bile-oleate-induced maximal increases in BF above control levels were 42±7%, 65±12%, and 58±8%, respectively. The observed inhibitory effect of L-NNA on the intestinal hyperaemic response to the bile-oleate mixture was reversed by pretreatment with L-arginine (100 mg/kg i.V.). In capsaicin pretreated rats the subsequent bile-oleate-induced hyperaemia was reduced in magnitude but the inhibitory effects of L-NNA were proportionately the same as in animals not receiving capsaicin. These findings support the hypothesis that NO is involved with bile-oleate-induced mesenteric hyperaemia.

Key words

Nitric oxide Intestinal circulation Postprandial hyperaemia Sensory neuropeptides Capsaicin L-NNA