| Project/Area Number |
13670724
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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 |
Circulatory organs internal medicine
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| Research Institution | Kyushu University |
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Principal Investigator |
HIRAKAWA Yoji Kyushu Univ, Dept of CV Med, Assist Prof, Hospital, 医学部附属病院, 助手 (90332840)
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| Co-Investigator(Kenkyū-buntansha) |
SHIMOKAWA Hiroaki Kyushu Univ, Dept of CV Med, Assoc Prof., 大学院・医学研究院, 助教授 (00235681)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2002: ¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 2001: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | EDHF / Vascular endothelial cells / EDRFs / Hydrogen peroxide / 内皮依存性過分極因子 / ブラジキニン / カタラーゼ / ギャップジャンクション |
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| Research Abstract |
We have recently identified that endothelium-derived hydrogen peroxide (H202) is an endothelium-derived hyperpolarizing factor (EDHF) in mice (Journal of Clinical Investigation, 2002). In this series of experiments, we have examined whether H202 is also and EDHF in human arteries.
In isolated human mesenteric arteries, EDHF-mediated responses were inhibited by catalase that specifically decomposes H202 into water and oxygen. Exopgenous H202 also exerted relaxations and hyperpolarizations of vascular smooth muscle. By contrast, we were unable to confirm other hypotheses on the nature of EDHF, including epoxyeicosatrienoic acids (EETs), K ion, and gap junctions.
These results indicate that H202 is also an EDHF in human mesenteric arteries.
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