Mechanism of acid-induced mesenteric hyperemia in rats

Kyoji Seno, Fumihiro Iwata, Kan Lam, Joseph Leung, Felix W. Leung

Research output: Contribution to journalArticlepeer-review

19 Scopus citations


The mesenteric hyperemia induced by intraduodenal application of hydrochloric acid (HCl) is mediated in part by capsaicin-sensitive afferent nerves. Antagonist of capsaicin-sensitive receptors (capsazepine) and blocker of capsaicin-sensitive cation channels (ruthenium red) have been described. We employed these tools to dissect the mechanism of regulation of mesenteric hyperemia induced by intraduodenal administration of HCl. Subcutaneous 100 μmol/kg capsazepine or intraduodenal 0.1% ruthenium red was administered to pentobarbital anesthetized rats. Then, 2.5 ml/kg of 640 μM capsaicin or 0.1 N HCl was administered intraduodenally. The mesenteric hyperemic responses were recorded. The results demonstrated that in a dose that decreased the mesenteric hyperemia induced by intraduodenal capsaicin, capsazepine failed to attenuate the mesenteric vasodilatory effect of intraduodenal HCl. Ruthenium red significantly attenuated the mesenteric hyperemia after intraduodenal capsaicin and HCl. These in vivo data provide the first functional evidence for the existence of capsazepine-sensitive capsaicin receptors and cation channel complexes in the rat duodenal and intestinal mucosa. The capsaicin- and HCl-sensitive receptors are unlikely to be functionally identical in these locations. The ruthenium red-sensitive cation channels appear to mediate the capsaicin- and HCl-induced mesenteric hyperemia.

Original languageEnglish (US)
Pages (from-to)1653-1662
Number of pages10
JournalLife Sciences
Issue number18
StatePublished - Sep 25 1998


  • Capsaicin
  • Capsazepine
  • Duodenum
  • Intestine
  • Ruthenium red

ASJC Scopus subject areas

  • Pharmacology


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