| Project/Area Number |
09470011
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General physiology
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| Research Institution | Nagoya City University |
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Principal Investigator |
SUZUKI Hikaru Nagoya City University Medical School, Professor, 医学部, 教授 (80037548)
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| Co-Investigator(Kenkyū-buntansha) |
YAMAMOTO Yoshimichi Nagoya City University Medical School, Lecturer, 医学部, 講師 (80145755)
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| Project Period (FY) |
1997 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥12,600,000 (Direct Cost: ¥12,600,000)
Fiscal Year 1998: ¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 1997: ¥10,800,000 (Direct Cost: ¥10,800,000)
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| Keywords | Smooth muscle / Spontaneous activity / Internal Ca store / Membrane potential / Pacemaker cell / Gap junction / Slow wave / 自発活動 / 胃 / カルシウム / 歩調取り電位 |
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| Research Abstract |
The cellular mechanisms of generation of spontaneous activity in smooth muscle were investigated using the guinea-pig stomach. As the analysis of gap junction is important for understanding the pacemaking, experiments were carried out on gap junctions using microvessels.
Gastric muscles consisted of circular, longitudinal and interstitial cells, and each produced different patterns of electrical activity. The circular muscle preparation revealed transient depolarization which summed together to form a large regenerative potential. Depolarizing pulse evoked the regenerative potential with long delay (about 1 s), and the potential showed long refractoxy periods (15-20 s). Reduction of intracellular Ca ions by BAPTA or disfunction of SR by CPA abolished the regenerative potential. These responses were not affected by nifedipine. We speculate an involvement of unidentified channel for generation of the regenerative potential. Ca ions from SR were considered important.
Dissociation of electrical connections between endothelium and smooth muscle by 18-beta glycirrhetinic acid (GA) caused disappearance of acetylcholine-induced hyperpolarization in smooth muscle, and the results suggested that endothelium-dependent hyperpolarization may be produced an electrical signal from endothelium through gap junctions. The results indicated that it is possible to explain the EDHF-induced hyperpolarization without considering a humoral substance.
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