抄録
Contributions of COX-1 and COX-2 in basal and ACh-stimulated prostaglandin E2 (PGE2) release were studied in antral mucosa of guinea pig. PGE2 was released from antral mucosa spontaneously. Acetylcholine (ACh), which increases [Ca2+] i, increased the PGE2 release from antral mucosa in a dose dependent manner. COX-1 or COX-2, which generates PGE2 from arachidonic acid (AA), was regulated by [Ca2+]i. Basal and ACh-stimulated PGE2 release were increased by the addition of AA, and was inhibited by a PLA2 inhibitor and COX inhibitors. SC560 (100 nM, a selective inhibitor of COX-1) decreased ACh-stimulated PGE2 release without any decrease in basal PGE2 release, while ionomycin increased PGE2 release. NS398 (20 μM, a selective inhibitor of COX-2) decreased basal PGE2 release without any decrease in ACh-stimulated PGE2 release. Moreover, in isolated antral epithelial cells, SC560 inhibited ACh-stimulated-PGE2 releases, however, NS398 did not. Thus, in antral mucosa, basal PGE2 release is maintained via COX-2 of interstitial cells and ACh-stimulated PGE2 release is maintained via COX-1 of antral epithelial cells. These observations suggest that PGE2 released via COX-2 in the interstitial cells maintains an integrity of the resting antral mucosa and that released via COX-1 in antral epithelial cells maintains an autocrine mechanism, which enhances Ca2+-regulated exocytosis in ACh-stimulated antral mucosa, such as during meals. [J Physiol Sci. 2006;56 Suppl:S118]
