| Project/Area Number |
07457021
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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 pharmacology
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| Research Institution | The University of Tokyo |
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Principal Investigator |
IINO Masamitsu The University of Tokyo, Fac.of Med., Professor, 医学部(医), 教授 (50133939)
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| Project Period (FY) |
1995 – 1996
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| Project Status |
Completed (Fiscal Year 1996)
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| Budget Amount *help |
¥7,200,000 (Direct Cost: ¥7,200,000)
Fiscal Year 1996: ¥2,600,000 (Direct Cost: ¥2,600,000)
Fiscal Year 1995: ¥4,600,000 (Direct Cost: ¥4,600,000)
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| Keywords | Vascular smooth muscle / Calcium ion / Inositol trispohophate / Blood pressure regulation / Digital imaginf / Fluorescent Ca^<2+> indicator / Ca^<2+> channel antagonist / 蛍光カルシウム指示薬 |
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| Research Abstract |
Using cooled CCD camera or confocal laser scanning microscope, we carried out digital imaging of intracellular Ca^<2+> concentration of vascular smooth muscle cells within intact arterial tissue. Ca^<2+> indicator loaded arterial tissue was mounted in an experimental chamber on the stage of an inverted microscope and stimulated with field electrical stimulation or by solution exchange. We could observe Ca^<2+> concentration change within individual smooth muscle cells, and confirmed our previous results that the intracellular Ca^<2+> concentration change takes place as Ca^<2+> oscillations and waves when the arterial tissue was stimulated with the sympathetic nerve transmitter, noradrenaline. The current experimental system had a greater dynamic range than that in our previous measurements. We studied the effect of dihydropyridine Ca^<2+> channel antagonists on the Ca^<2+> oscillations. In the presence of nicardipine at a concentration enough to inhibit high K-induced intracellular Ca^<2+> increase in vascular smooth muscle cells the frequency of the noradrenaline-induced Ca^<2+> oscillation was significantly inhibited. This new finding suggest that Ca^<2+> channel antagonist can inhibit Ca^<2+> store-mediated Ca^<2+> signalling. We are now expanding our work and preparing for simultaneous measurement of intracellular Ca^<2+> concentrations of vascular smooth muscle cells and endothelial cells to study the effect of endothelium derived relaxing factor on the Ca^<2+> signalling in vascular smooth muscle cells.
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