| Project/Area Number |
13671645
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
Urology
|
|---|
| Research Institution | Department of Urology, Hamamatsu University School of Medicine |
|---|
Principal Investigator |
KAGEYAMA Shinji Assistant Professor, Department of Urology, Hamamatsu University School of Medicine, 医学部附属病院, 講師 (60224367)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
FUJITA Kimio Professor, Department of Urology, Hamamatsu University School of Medicine, 医学部, 教授 (80111813)
|
|---|
| Project Period (FY) |
2001 – 2002
|
| Project Status |
Completed (Fiscal Year 2002)
|
| Budget Amount *help |
¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2002: ¥1,200,000 (Direct Cost: ¥1,200,000)
|
|---|
| Keywords | ATP / Detrusor Overactivity / Prostaglangin E2 / Purinoceptor / calcium antagonist / Indeomethacin / COX-2 antagonist / 尿失禁 |
|---|
| Research Abstract |
Recently, ATP is shown to act as a main non-adrenergic non-cholinergic neurotransmitter in bladder behavior. In aged bladder, detrusor overactivity caused clinically to urinary frequency and urge incontinence. We reported that ATP sensitivity is increased in aged rat bladder via prostaglandin E2, which was related to irritative symptoms in urinary tracts.
We study bladder sensory hypersensitivity for making aged bladder model with rat by amyloid presusor protein rich feeding. Then, urinary bladders from this aged detrusor overactivity model were experimented with various neuroagents, such as PGE2, purinoceptor antagonists, calcium antagonists, COX-2 antagonist, and indomethacin.
This project is not finished successfully for making aged detrusor overactivity model, however we demonstrated that ATP-induced detrusor muscle contraction was complicated both mucarinic receptor and aged muscle change. Further experiments are needed for clarifying the detrusor overactivities in aged rats and human.
|
