The investigation into the molecular and electrophysiological properties of overactive bladder and the research for the novel consequent treatment

膀胱过度活动症的分子和电生理特性研究及后续治疗新方法的研究

• 批准号: 20599012
• 负责人: KAJIOKA Shunichi
• 金额: $ 2.52万
• 依托单位: Kyushu University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2008
• 资助国家: 日本
• 起止时间: 2008 至 2010
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-20599012/
• 关键词: 膀胱排尿筋; 過活動膀胱; イオンチャネル; 特殊間質性細胞; カルシウムオシレーション; 特殊間質性細

The molecular and electrophysiological properties of ATP-sensitive K+ channel were clarified in pig detrusor smooth muscle (Kajioka et al. J Pharmacol Exp Ther 2008). Also in human detrusor smooth muscle, the single channel current of ATP-sensitive K+channel were successfully recorded and this channel was activated by β-nicotinamide adenine dinucleotide (βNAD) (Kajioka et al. J Urol 2011 in press).Western Blotting and immunohistochemical staining failed to reveal the significant predominant increase of ckit-positive interstitial cell or gap junction in the outlet obstruction bladder of guinea pig. However, immunohistochemical staining demonstrated that the expression of both M2 and M3 muscarinic receptor subtypes were increased by the obstruction. As for Ca2+ sensitization in human detrusor, we concluded that M3 receptor had a predominant role and comparable contribution to ROK and PKC pathways while it M2 receptor mediated ROK pathway via the down regulation of cAMP.

在猪逼尿肌平滑肌中阐明了ATP敏感性K+通道的分子和电生理学特性（Kajioka et al. J Pharmacol Exp Ther 2008）。同样在人逼尿肌平滑肌中，成功记录了ATP敏感性K+通道的单通道电流，并且该通道被β-烟酰胺腺嘌呤二核苷酸（βNAD）激活（Kajioka et al. J Urol 2011 in press）蛋白质印迹和免疫组织化学染色未能揭示豚鼠出口梗阻膀胱中ckit阳性间质细胞或间隙连接的显著主要增加。免疫组织化学染色显示，M2和M3受体亚型的表达均增加。在逼尿肌Ca ~（2+）敏感化中，M_3受体对ROK和PKC通路起主导作用，而M_2受体通过下调cAMP介导ROK通路。

项目成果

Bladder outlet obstruction modulates Ca2+ sensitization in α toxin permeabilized guinea pig detrusor smooth muscle.

膀胱出口梗阻调节 α 毒素透化豚鼠逼尿肌平滑肌中的 Ca2+ 敏化。

• 发表时间: 2010
• 作者: Nouval S;Kajioka S;Seki N;Naito S
• 通讯作者: Naito S

ヒト膀胱排尿筋のATP感受性Kチャネルは、β-nicotine amide adenine dinucleotide (βNAD)によって活性化される

人膀​​胱逼尿肌中 ATP 敏感 K 通道被 β-烟碱酰胺腺嘌呤二核苷酸 (βNAD) 激活

• 发表时间: 2009
• 作者: 梶岡俊一;他
• 通讯作者: 他

Etiology of overactive bladder and its therapeutic perspective-focusing on a myogenic basis for the overactive bladder.

膀胱过度活动症的病因学及其治疗观点——重点关注膀胱过度活动症的肌源性基础。

• 发表时间: 2010
• 期刊: Fukuoka Igaku Zasshi. 101(5)(review)
• 作者: Kajioka S;Seki N;Shahab N;Yunoki T;Naito S.
• 通讯作者: Naito S.

The profiles and patterns of detrusor overactivity and their association with overactive bladder symptoms in men with benign prostatic enlarge ment associated with detrusor overactivity

男性良性前列腺肥大与逼尿肌过度活动的逼尿肌过度活动的概况和模式及其与膀胱活动过度症状的关联

• 发表时间: 2009
• 期刊: Neurourology & Urodynamics (印刷中)
• 作者: Shahab N;Seki N;Takahashi R Kaiioka S;Takei M;Yamaguchi A;Naito S
• 通讯作者: Naito S

-nicotineamide adenine dinucleotide activates an ATP-sensitive potassiumss channel of human urinary bladder

-烟酰胺腺嘌呤二核苷酸激活人膀胱的ATP敏感钾通道

• 发表时间: 2009
• 作者: 梶岡俊一;Nouval Shahab;森田浩光;杉原恵美;Alison Brading;関成人;内藤誠二
• 通讯作者: 内藤誠二