MECHANISMS OF BLADDER EP1THELIUM INDUCE PAIN SENSATION
Project/Area Number |
21600001
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
疼痛学
|
Research Institution | Akita University |
Principal Investigator |
|
Co-Investigator(Kenkyū-buntansha) |
MIYAI Kazumasa 秋田大学, 大学院・医学系研究科, 准教授 (60283933)
ITO Tomoko 秋田大学, 大学院・医学系研究科, 教授 (50241675)
YOSHIZUMI Masaru 秋田大学, 大学院・医学系研究科, 助教 (70553379)
|
Project Period (FY) |
2009 – 2011
|
Project Status |
Completed (Fiscal Year 2011)
|
Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2011: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2010: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2009: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
|
Keywords | 膀胱痛 / TRPV1 / ATP / 上皮細胞 / 膀胱 / 痛み / パルスレーザー照射 / 炎症 / 頻尿 / ノルアドレナリン / 脊髄 / 排尿中枢 / プロスタグランジン / 求心性神経線維 |
Research Abstract |
ATP secretion from the urinary bladder was observed pressure dependently (from 5cmH_2O to 45cmH_2O). Stimulation of either TRPV1 channel, EP1 receptor (Prostaglandin E_2 receptor) or muscarinic receptor increased ATP secretion which releasing Ca^<2+> from endoplastic reticulum. Activation of adenylate cyclase also increased ATP secretion which independent from previous mechanism. Store-operated Ca^<2+> entry suppressed distention-induced ATP release from urothelim. These could be important for continuous ATP release during the storage of the urine in the urinary bladder.
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Report
(4 results)
Research Products
(41 results)