作者: Sasaki Y , Takeuchi K , Ise F , Aihara E , Nomura Y
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摘要: We investigated the cyclooxygenase (COX) isoforms as well prostaglandin E receptor EP subtypes responsible for acid-induced gastric HCO(3)(-) secretion in rats and receptor-knockout (-/-) mice. Under urethane anesthesia, a chambered stomach (in presence of omeprazole) was perfused with saline, measured at pH 7.0 using pH-stat method by adding 2 mM HCl. Mucosal acidification achieved exposing 10 min to 50 or 100 Acidification mucosa increased both WT mice, an indomethacin-inhibitable manner. The inhibited prior administration indomethacin SC-560 but not rofecoxib PGE(2) content rat stomach, this response significantly attenuated rofecoxib. This also ONO-8711 (EP1 antagonist) AE3-208 (EP4 disappeared EP1 EP3 action These results support mediator role endogenous PGs induced mucosal clearly indicate that enzyme production process is COX-1. They further show receptors essential increase stomach.