IP3R介导的钙释放在DI发生中的作用研究  

Role of IP3R mediated Ca^(2+) release in detrusor instability

作　　者：郑霁[1] 方强[1] 陈志文[1] 陈志朋[1] 何鹏[1] 邓国贤[1] 代林勇 潘进洪[1] 

机构地区：[1]第三军医大学西南医院.全军泌尿外科研究所,重庆400038

出　　处：《西部医学》2015年第2期167-169,共3页Medical Journal of West China

基　　金：国家自然科学基金青年基金(NSFC81100539)

摘　　要：目的探讨IP3R的功能改变是否参与了逼尿肌不稳定(DI)的发生。方法对比分析DI和对照组大鼠膀胱平滑肌IP3R mRNA和蛋白表达的变化,观察IP3R阻断剂Heparin对DI和对照组膀胱平滑肌条收缩幅度和频率的影响。结果 DI逼尿肌细胞IP3RmRNA和蛋白表达较对照组显著增加。IP3R阻断剂Heparin能显著抑制DI、正常组大鼠逼尿肌肌条自发收缩频率及收缩幅度,且Heparin对DI逼尿肌条的影响效应要显著高于正常组。结论 IP3R功能在DI逼尿肌组织兴奋、收缩发生中明显上调,这种上调在DI的发生中起着重要作用。Objective To investigate the role of IP3 R mediated Ca^2＋ release in detrusor instability.Methods The expression of IP3 R mRNA and protein were tested from rat detrusor of DI and control group group.The effect of IP3 R blocker heparin on detrusor strips were then recorded for further analysis.Results Compared with control group,the expression of IP3 R mRNA and protein were significantly increased in detrusor strips from DI group.Heparin can significantly inhibited the frequency and amplitude of spontaneous contractile activity in both the DI and control strips.The inhibit effect by heparin was more obvious in DI group.Conclusion The elevated expression and function of IP3 Rcontributed to detrusor instability.

关 键 词：IP3R 钙离子通道 逼尿肌不稳定 尿动力学 

分 类 号：R446.8[医药卫生—诊断学]