| Project/Area Number |
26861258
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
Urology
|
|---|
| Research Institution | The University of Tokyo |
|---|
Principal Investigator |
Aizawa Naoki 東京大学, 医学部附属病院, 特任助教 (80595257)
|
|---|
| Project Period (FY) |
2014-04-01 – 2016-03-31
|
| Project Status |
Completed (Fiscal Year 2015)
|
| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2015: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2014: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
|
|---|
| Keywords | 求心性神経 / 膀胱 / 下部尿路閉塞 / ラット / 内因性カンナビノイド / 膀胱微小収縮 / 下部尿路機能障害 |
|---|
| Outline of Final Research Achievements |
We investigated the effect of several drugs on single-unit afferent activities (SAAs) of the bladder mechanosensitive primary afferent nerve fibers in rats. The study demonstrated that both α1A- and 1D adrenoceptors in the rat bladder are involved in the activation of the bladder Aδ-fibers during bladder filling. In addition, we demonstrated that enhanced peripheral endocannabinoids reduces C-fiber hyperactivity in the rat bladder provoked by PGE2.
We also evaluated the characteristics of mechanosensitive SAAs in the bladder in a male rat model of bladder outlet obstruction (BOO), and their relationship with microcontractions. The results indicate that the SAAs of Aδ-fibers were attenuated, but the SAAs of both Aδ- and C-fibers were intermittently enhanced by propagation of microcontractions during bladder filling in male rats with BOO. These findings support the view that microcontractions contribute to the development of urgency and/or detrusor overactivity associated with BOO.
|
