2003 Fiscal Year Final Research Report Summary
The Mechanisms of signal transduction and Development in Interstitial cells of Cajal
| Project/Area Number |
14571206
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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 |
Digestive surgery
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| Research Institution | Kyushu University |
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Principal Investigator |
MASUMOTO Kouji Kyushu University Hospital, Assistant professor, 大学病院, 講師 (20343329)
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| Co-Investigator(Kenkyū-buntansha) |
SHONO Takeshi Kyushu University Hospital, Assistant professor, 大学病院, 講師 (30235717)
TAGUCHI Tomoaki Kyushu University Hospital, Assistant professor, 大学病院, 助教授 (20197247)
SUITA Sachiyo Kyushu University Hospital, Professor, 大学病院, 教授 (30038856)
IEIRI Satoshi Kyushu University Hospital, Assistant professor, 大学病院, 助手 (00363359)
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| Project Period (FY) |
2002 – 2003
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| Keywords | Neurokinin A / [Ca^<2+>]i / Ca^<2+> sensitivity / Rho kinase / guinea-pig / Ca^<2+> channel / smooth muscle cells / Fura-2 |
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| Research Abstract |
1 The mechanisms for the contraction induced by neurokinin A (NKA) in the smooth muscle of guinea-pig taenia coil were investigated by means of simultaneous measurements of intracellular Ca^<2+> concentration ([Ca^<2+>]i) and tension.
2 NKA (100 pM -10 □M) caused a concentration -dependent contraction. A maximum response was obtained at 1 □M and the EC50 value was 84.1±12.9 nM.
3 While the rise in [Ca^<2+>]i induced 1 μM NKA was similar to an increase in [Ca^<2+>]i induced by 60 mM K^+ PSS depolarization, the developed force during the contraction induced 1 μM NKA was significantly larger than that of 60 mM K^+ PSS depolarization.
4 Both the L-type Ca^<2+> channel blocker, diltiazem and the NK2 receptor selective antagonist, NK2-ra significantly inhibited the NKA induced [Ca^<2+>]i elevation and contraction. The NK1 receptor selective antagonist, TAK637 had no effect on the NKA induced contraction.
5 Neurokinin A induced only transient increases in [Ca^<2+>]i and force in a Ca^<2+> -free solution in smooth muscle of guinea-pig taenia coli.
6 We compared [Ca^<2+>]i and the force development induced by NKA only with [Ca^<2+>]i and the force induced in NKA in the presence of Rho kinase inhibitor, Y-27632. Y-27632 significantly inhibited the NKA induced force development, while had no influense on [Ca^<2+>]i elevation.
7 In conclusion, NKA induces the contraction of the guinea-pig taenia coli by increasing in [Ca^<2+>]i as well as increasing Ca^<2+> sensitivity of contractile apparatus. NKA induced increases in [Ca^<2+>]i are caused by Ca^<2+> influx via voltage -dependent Ca^<2+> channels, NK2 receptor -operated Ca^<2+> channels, and Ca^<2+> release from sarcoplasmic reticulum, (SR). Contraction induced by NKA was enhanced through the Rho kinase passway. We suggested that the contractile mechanism exclude [Ca^<2+>]i elevation could exsist in the smooth muscle of guinea-pig taenia coli.
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