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자료유형
학술저널
저자정보
한종수 (중앙대학교) 민영실 (중원대학교) 김길형 (중앙대학교 약학과) 채상현 (중앙대학교) 남윤진 (중앙대학교) 이재휘 (중앙대학교) 이석용 (성균관대학교) 손의동 (중앙대학교)
저널정보
대한약리학회 The Korean Journal of Physiology & Pharmacology The Korean Journal of Physiology & Pharmacology 제22권 제5호
발행연도
2018.9
수록면
577 - 584 (8page)
DOI
https://doi.org/10.4196/kjpp.2018.22.5.577

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Bladder dysfunction is a common complication of diabetes mellitus (DM). However, there have been a few studies evaluating bladder smooth muscle contraction in DM in the presence of pharmacological inhibitors. In the present study, we compared the contractility of bladder smooth muscle from normal rats and DM rats. Furthermore, we utilized pharmacological inhibitors to delineate the mechanisms underlying bladder muscle differences between normal and DM rats. DM was established in 14 days after using a single injection of streptozotocin (65 mg/kg, intraperitoneal) in Sprague-Dawley rats. Bladder smooth muscle contraction was induced electrically using electrical field stimulation consisting of pulse trains at an amplitude of 40 V and pulse duration of 1 ms at frequencies of 2-10 Hz. In this study, the pharmacological inhibitors atropine (muscarinic receptor antagonist), U73122 (phospholipase C inhibitor), DPCPX (adenosine A1 receptor antagonist), udenafil (PDE5 inhibitor), prazosin (a1-receptor antagonist), verapamil (calcium channel blocker), and chelerythrine (protein kinase C inhibitor) were used to pretreat bladder smooth muscles. It was found that the contractility of bladder smooth muscles from DM rats was lower than that of normal rats. In addition, there were significant differences in percent change of contractility between normal and DM rats following pretreatment with prazosin, udenafil, verapamil, and U73122. In conclusion, we suggest that the decreased bladder muscle contractility in DM rats was a result of perturbations in PLC/IP3-mediated intracellular Ca2+ release and PDE5 activity.

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