QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: jpet.105.087619v1 315/1/423    most recent Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Aihara, E. Articles by Takeuchi, K. Search for Related Content PubMed PubMed Citation Articles by Aihara, E. Articles by Takeuchi, K.

GASTROINTESTINAL, HEPATIC, PULMONARY, AND RENAL

Mechanisms Underlying Capsaicin-Stimulated Secretion in the Stomach: Comparison with Mucosal Acidification

Department of Pharmacology and Experimental Therapeutics, Kyoto Pharmaceutical University Misasagi, Yamashina, Kyoto, Japan

The effects of capsaicin and mucosal acidification on gastric secretion were compared in wild-type and prostacyclin (PGI₂) IP receptor or prostaglandin E receptor EP1 or EP3 knockout C57BL/6 mice as well as rats. Under urethane anesthesia, the stomach was mounted on an ex vivo chamber, perfused with saline, and the secretion of was measured at pH 7.0 using the pH-stat method. Capsaicin or 200 mM HCl was applied to the chamber for 10 min. Capsaicin increased the secretion of in rats and wild-type mice, the response at 0.3 mg/ml being equivalent to that induced by acidification. This effect of capsaicin in rats was abolished by ablation of capsaicin-sensitive afferent neurons and attenuated by indomethacin, N^G-nitro-L-arginine methylester (L-NAME), and capsazepine [transient receptor potential vanilloid type 1 (TRPV1) antagonist] but not FR172357 [3-bromo-8-[2,6-dichloro-3-[N[(E)-4-(N,N-dimethylcarbamoyl) cinnamidoacetyl]-N-methylamino]benzyloxy]-2-metylimidazo[1,2-a]pyridine; bradykinin B2 antagonist] or the EP1 antagonist. The acid-induced secretion was attenuated by indomethacin, L-NAME, the EP1 antagonist, and sensory deafferentation, but not affected by capsazepine or FR172357. Prostaglandin E₂ (PGE₂), NOR-3 [(±)-(E)-ethyl-2-[(E)-hydroxyimino]-5-nitro-3-hexeneamine] (NO donor), and bradykinin stimulated the secretion of , and the effect of bradykinin was blocked by indomethacin and L-NAME as well as FR172357. The stimulatory effect of capsaicin disappeared in IP (-/-) mice, whereas that of acidification disappeared in EP1 (-/-) mice. Intragastric application of capsaicin increased mucosal PGI₂ but not PGE₂ levels in the rat stomach. These results suggested that both capsaicin and acid increase gastric secretion via a common pathway, involving PG and NO as well as capsaicin-sensitive afferent neurons, yet their responses differ concerning TRPV1 or prostanoid receptor dependence.

Address correspondence to: Dr. Koji Takeuchi, Department of Pharmacology and Experimental Therapeutics, Kyoto Pharmaceutical University, Misasagi, Yamashina, Kyoto 607, Japan. E-mail: takeuchi{at}mb.kyoto-phu.ac.jp

This article has been cited by other articles:

				K. Kita, K. Takahashi, Y. Ohashi, H. Takasuka, E. Aihara, and K. Takeuchi Phosphodiesterase Isozymes Involved in Regulation of Formula Secretion in Isolated Mouse Stomach in Vitro J. Pharmacol. Exp. Ther., September 1, 2008; 326(3): 889 - 896. [Abstract] [Full Text] [PDF]