1993 Fiscal Year Final Research Report Summary
Signal transduction mechanisms operated via receptor activation in the smooth muscle
| Project/Area Number |
04660322
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
基礎獣医学
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| Research Institution | Gifu University |
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Principal Investigator |
KOMORI Seiichi Gifu Univ., Faculty of Agriculture, Associate Professor, 農学部, 助教授 (70195866)
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| Co-Investigator(Kenkyū-buntansha) |
TAKEWAKI Tadashi Gifu Univ., The United Graduate School of Veterinary Sciences (Doctoral Course),, 大学院・連合獣医学研究科, 教授 (00021717)
OHASHI Hidenori Gifu Univ., Faculty of Agriculture, Professor, 農学部, 教授 (40001531)
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| Project Period (FY) |
1992 – 1993
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| Keywords | Smooth muscle / Histamine / G protein / Cationic channel / Calcium stores / Muscarinic receptor / Inositol triphosphate / Membrane current |
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| Research Abstract |
The present study was to investigate the effects of carbachol and histamine on membrane currents in single smooth muscle cells of guinea-pig ileum using a patch-clamp technique and on tension in beta -escin-skinned smooth muscle of the same intesitine, in an attempt to elucidate signal transduction systems involved in both activation of cationic channels and release of Ca^<2+> stores brought about by stimulation of eigher muscarinic or histamine receptors.
1. Both cationic current and Ca^<2+>-store release elicited by histamine are indistinguishable in pharmacological properties from those elicited by carbachol.
2. A G-protein system plays a role in each of the two cellular responses to either receptor stimulation, but a G-protein involved in the release of Ca^<2+> stores is characterized by insensitivity to pertussis toxin.
3. Both receptor agonists act on caffeine-sensitive stores to release Ca^<2+> via formation of inositol trisphosphate (IP3).
4. The cationic current in response to receptor stimulation is potentiated by a rise in cytosolic Ca^<2+> due to release of Ca^<2+> stores. Generation of oscillations in the cationic current may involve cyclical release of Ca^<2+> stores which is triggerd by IP3 formed during receptor stimulation.
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