2012 Fiscal Year Final Research Report
The mechanism of inhibitory effect of AMP kinase for aldosterone-induced vascular damage
| 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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| Keywords | 血管病態学 |
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| 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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