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This Article Full Text Full Text (PDF) All Versions of this Article: 91/6/1015    most recent expphysiol.2006.034405v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend 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 Shimamoto, C. Articles by Nakahari, T. Search for Related Content PubMed PubMed Citation Articles by Shimamoto, C. Articles by Nakahari, T.

¹ Central Research Laboratory (Nakahari Project)² Department of Internal Medicine (Division of Gastroenterology)³ Department of Microbiology⁴ Department of Physiology⁵ Department of Pathology, Osaka Medical College, 2-7 Daigaku-cho, Takatsuki 569-8686, Japan

Prostaglandin E₂ (PGE₂), which is generated by two isoforms of cyclo-oxygenase (COX₁ and COX₂), is a key mediator in gastric mucosal defense. In the present study, antral mucosa of guinea-pigs was incubated with various agonists or antagonists in a medium, the PGE₂ concentration of which was measured using a PGE₂ EIA kit. Prostaglandin E₂ was released from the antral mucosa spontaneously (basal PGE₂ release) and acetylcholine (ACh, 10 µM) enhanced the PGE₂ release (ACh-stimulated PGE₂ release) was mediated via intracellular Ca²⁺ concentration ([Ca²⁺]_i). Arachidonic acid enhanced both forms of PGE₂ release, and a phospholipase A₂ inhibitor (amylcinnamoyl anthranilic acid) and COX inhibitors (acetylsalicylic acid and indomethacin) decreased them. 5-(4-Chlorophenyl)-1-(4-methoxyphenyl)-3-trifluoromethylpyrazol (SC560, 100 nM, a COX₁-selective inhibitor) inhibited ACh-stimulated PGE₂ release without any decrease in basal PGE₂ release. N-(2-Cyclohexyloxy-4-nitrophenyl) methanesulphonamide (NS398, 20 µM, a COX₂-selective inhibitor) decreased basal PGE₂ release without any reduction of ACh-stimulated PGE₂ release. However, ionomycin (a Ca²⁺ ionophore) increased PGE₂ release from antral mucosa in the presence of SC560 or NS398, suggesting that COX₁ and COX₂ are regulated by [Ca²⁺]_i. These findings indicate that COX₁-containing cells have ACh receptors but COX₂-containing cells do not. Moreover, in isolated antral epithelial cells, SC560 decreased basal and ACh-stimulated PGE₂ release, but NS398 did not. In conclusion, in antral mucosa, basal PGE₂ release is mainly maintained by COX₂ of non-epithelial cells, and ACh-stimulated PGE₂ release is maintained by COX₁ of epithelial cells.

(Received 5 May 2006; accepted after revision 29 August 2006; first published online 31 August 2006)
Corresponding author T. Nakahari: Department of Physiology, Osaka Medical College, 2–7 Daigaku-cho, Takatsuki 569-8686, Japan. Email: takan{at}art.osaka-med.ac.jp

This article has been cited by other articles:

				C. Shimamoto, E. Umegaki, K.-i. Katsu, M. Kato, S. Fujiwara, T. Kubota, and T. Nakahari [Cl ]i modulation of Ca2+-regulated exocytosis in ACh-stimulated antral mucous cells of guinea pig Am J Physiol Gastrointest Liver Physiol, October 1, 2007; 293(4): G824 - G837. [Abstract] [Full Text] [PDF]