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Am J Physiol Gastrointest Liver Physiol 277: G268-G274, 1999;
0193-1857/99 $5.00
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Vol. 277, Issue 2, G268-G274, August 1999

Acid-sensing pathways of rat duodenum

Yasutada Akiba1,2, Paul H. Guth3, Eli Engel4, Igor Nastaskin1, and Jonathan D. Kaunitz1,2,3

3 West Los Angeles Veterans Affairs Medical Center, 1 CURE: Digestive Diseases Research Center, 2 Department of Medicine, School of Medicine, and 4 Department of Biomathematics, University of California, Los Angeles, California 90073

We tested the hypothesis that the duodenal hyperemic response to acid occurs through activation of capsaicin-sensitive afferent nerves with subsequent release of vasodilatory substances such as calcitonin gene-related peptide (CGRP) and nitric oxide (NO). Laser-Doppler flowmetry was used to measure duodenal blood flow in urethan-anesthetized rats. Duodenal mucosa was superfused with pH 7.0 buffer with capsaicin or bradykinin or was acid challenged with pH 2.2 solution, with or without vanilloid receptor antagonists, a CGRP receptor antagonist, an NO synthase (NOS) inhibitor, or a cyclooxygenase inhibitor. The selective vanilloid receptor antagonist capsazepine (CPZ) dose dependently inhibited the hyperemic response to acid and capsaicin but did not affect bradykinin-induced hyperemia. Ruthenium red was less inhibitory than capsazepine. Selective ablation of capsaicin-sensitive nerves, CGRP-(8---37), and NG-nitro-L-arginine methyl ester inhibited acid-induced hyperemia, but indomethacin did not. We conclude that luminal acid, but not bradykinin, stimulates CPZ-sensitive receptors on capsaicin-sensitive afferent nerves of rat duodenum. Activation of these receptors produces vasodilation via the CGRP-NO pathway but not via the cyclooxygenase pathway. Acid appears to be the endogenous ligand for duodenal vanilloid receptors.

laser-Doppler flowmetry; vanilloid (capsaicin) receptor; capsazepine; bradykinin; indomethacin


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