2011 Fiscal Year Final Research Report
MECHANISMS OF BLADDER EP1THELIUM INDUCE PAIN SENSATION
| Project/Area Number |
21600001
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
疼痛学
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| Research Institution | Akita University |
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Principal Investigator |
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| 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)
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| Project Period (FY) |
2009 – 2011
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| Keywords | 膀胱痛 / TRPV1 / ATP / 上皮細胞 |
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| 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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