We investigated the presence of EP
1 receptor in the urothelium and its role in micturition reflex by examining the effect of intravesical administration of prostaglandin E
2 (PGE
2), an EP
1 agonist (ONO-DI-004), acetic acid, and capsaicin. Age-matched EP
1-KO mice and C57BL/6 wild-type (WT) mice were used. Western blots and standard immunohistochemical procedures were performed. Cystometrygram (CMG) was performed without anesthesia in a restraining cage. ATP release from the cultured urothelium cells was performed using luciferin-luciferase luminometry. The EP
1 receptor was found to be present in the urothelium. In WT mice, PGE
2 infusion shortened the intercontraction interval (ICI) in a dose-dependent fashion; however, it did not alter the ICI in EP
1-KO mice. The EP
1 agonist significantly shortened the ICI in WT mice, but not in EP
1-KO mice. Acetic acid and capsaicin shortened the ICI in both WT mice and EP
1-KO mice. EP
1 agonist, PGE
2 and capsaicin provoked ATP release from cultured urothelial cells. These results suggest that EP
1 receptor was present in bladder urothelium, and could be activated by PGE
2 to release ATP. EP
1 receptor in urothelium might be important for reflex voiding in pathological conditions.
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