1996 Fiscal Year Final Research Report Summary
NO production in endothelial cells and macropgage via a Cl^- channel
| Project/Area Number |
07457175
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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 |
Circulatory organs internal medicine
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| Research Institution | Tokyo Metropolitan Institute of Gerontology |
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Principal Investigator |
UEDA Seigo Tokyo Metropolitan Institute of Gerontology, Cell Biology, Fellow, 細胞生物学部門, 研究員 (00160169)
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| Project Period (FY) |
1995 – 1996
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| Keywords | endothelial cells / Cl^- channel / protein kinase A / cAMP / Ca^<2+> / NO / プロテインキナーゼA / SHR |
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| Research Abstract |
We reported that endothelial cells have a Cl^- channel, which is activated by cAMP (Circ Res 1990) and adenosine Al receptor agonist (Jpn Circ J). This type of a Cl^- channel mediate elevation of intracellular Ca^<2+> concentration. We investigated the effect of a Cl^- channel on No production of endothelial cells. Bovine pulmonary endothelia cells were grown in 35 mm culturedishes Intracellular Ca^<2+> concentration was measured by ARGUS system, using Fura 2/AM.No was was measured ny NO-sensitve electrode (WPI Co.). cAMP or adenosine caused elevation of tracellular Ca^<2+> concentration in a dose dependent manner. cAMP or adenosine also produced NO in endothelial cells. Increase in NO content in endothelial cells depended on extracellular Ca^<2+> concentration. teh present study suggests that a Cl^- channel mediates No production of endothelial cells.
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Research Products
(10 results)
