抄録
Previous study indicated that activation of adrenergic α1 receptor in urothelium induced ATP release, which was thought as a trigger of micturition reflex. However, the relevance of α1 receptor in urothelium to the structure and the motility is remained to be elucidated. Here we explored the influence of activation of α1 receptor on morphology and motility in urothelium using primary cell culture system. The role of α1 receptor was estimated with cell staining, time lapse analysis and wound healing assay. High dose of phenylephrine (10μM) rapidly induced morphological change in urothelium, especially in the peripheral region formed with pseudopodia and lamellipodia, revealed by F-action and paxillin staining. From the time lapse analysis, the motility was significantly increased by phenylephrine (10nM), while it was not significantly increased by isoproterenol (10nM). The healing from the wound was dose-dependently ameliorated by the phenylephrine (0.01 nM to 10 nM). The amelioration induced by phenylephrine was inhibited by the addition of α1 non-selective-antagonist, prazocin (1 nM), and α1A selective-antagonist, silodosin (1 nM). The density of pseudopodia and nucleus on the wounded edge was significantly increased after phenylephrine treatment. Both responses were inhibited by pretreatment of silodosin (1 nM). These results indicated that activation of α1A receptor caused the proliferation and the motility of urothelium on wound healing process through morphological change. The pathophysiological process of neurogenic cystitis might be depend on α1A receptor of urothelium. [J Physiol Sci. 2008;58 Suppl:S205]
