| Project/Area Number |
22590823
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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 | Dokkyo Medical University (2011-2012)
The University of Tokyo (2010) |
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Principal Investigator |
|
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| Co-Investigator(Renkei-kenkyūsha) |
TANAKA Kimie 東京大学, 保健センター, 助教 (30508065)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2012: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2011: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2010: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | 血管病態学 / AMPキナーゼ / 血管内皮 / アルドステロン / ミネラロコルチコイド / 一酸化窒素 / 血管 / 動脈硬化 |
|---|
| Research Abstract |
We succeeded in creating vascular-endothelium-specific dominant-negative (dn) and constitutively-active (ca) AMPK transgenic mice using Tet-On expression system. In DOX-treated DOCA-salt TEK-rtTA/TRE-caAMPK mice, endothelium-dependent vasodilatation was significantly ameliorated compared to control DOCA-salt mice. L-NMMA pretreatment to inhibit eNOS completely canceled such ameliorating effect. Endothelium-dependent vasodilatation was significantly attenuated in DOX-treated DOCA-salt TEK-rtTA/TRE-dnAMPK mice thanin control mice. The blood pressure levels of three types DOCA-salt mice (Wt, caAMPK, dnAMPK) were not different, suggesting that such endothelial-protective effect of AMPK was BP-independent.
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