Involvement of prostaglandin E receptor EP3 subtype and prostacyclin IP receptor in decreased acid response in damaged stomach

• Autorzy: Nishio H. , Terashima S. , Nakashima M. , Aihara E. , Takeuchi K.
• Języki publikacji: EN

Abstrakty

EN

We investigated the roles of cyclooxygenase (COX) isozymes and prostaglandin E (PGE) receptor EP1 and EP3 subtypes or prostacyclin IP receptors in the decrease in acid secretion in the damaged mouse stomach. Male C57/BL6 mice, both wild type and animals lacking EP1, EP3, or IP receptors, were used after 18 h of fasting. Under urethane anesthesia, the stomach was mounted on an ex-vivo chamber and perfused with saline, and acid secretion as well as transmucosal potential difference (PD) was measured before and after exposure to 20 mM taurocholate Na (TC) for 20 min. Indomethacin, SC-560 or rofecoxib was given i.d. 30 min before TC. Mucosal exposure to TC in wild-type mice caused a reduction in PD, followed by decrease in acid secretion. Indomethacin attenuated the decrease in acid secretion after exposure to TC in wild-type mice, an effect mimicked by SC-560 but not rofecoxib, yet none of these drugs affected the decrease in PD. An altered acid response after exposure to TC was similarly observed in EP1 (-/-) mice but mitigated in mice lacking either EP3 or IP receptors, although a decrease in PD was observed in all groups. Furthermore, the decreased acid response was also attenuated by prior administration of the EP3- but not EP1- antagonist. Mucosal levels of PGE2 and 6-keto PGF1alpha increased after exposure to TC in all groups of mice. In conclusion, the decrease in acid secretion in the damaged stomach is mediated by endogenous PGs derived from COX-1, through PGE2/EP3 receptors and prostacyclin/IP receptors.

Słowa kluczowe

EN

prostaglandin EP receptor; acid secretion; prostaglandin E; isoenzyme; prostacyclin; IP receptor; damaged stomach; cyclooxygenase; stomach; rat; EP3 receptor

• Wydawca: -
• Czasopismo: Journal of Physiology and Pharmacology
• Rocznik: 2007
• Tom: 58
• Numer: 3
• Opis fizyczny: p.407-421,fig.,ref.

Twórcy

autor

Nishio H.

• Kyoto Pharmaceutical University, Misasagi, Yamashina, Kyoto 607, Japan

autor

Terashima S.

autor

Nakashima M.

autor

Aihara E.

autor

Takeuchi K.