Endothelium-derived hyperpolarizing factor in pulmonary artery hypertension
Project/Area Number |
25461621
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Pediatrics
|
Research Institution | The University of Tokushima |
Principal Investigator |
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Co-Investigator(Kenkyū-buntansha) |
SAKATA Miho 徳島大学, 病院, 特任助教 (80532514)
|
Project Period (FY) |
2013-04-01 – 2016-03-31
|
Project Status |
Completed (Fiscal Year 2015)
|
Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2015: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2014: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
|
Keywords | 肺高血圧症 / 肺動脈 / 血管内皮由来過分極因子 / チャネル / カリウムチャネル / 血管 / 内皮細胞 / 平滑筋細胞 |
Outline of Final Research Achievements |
Pulmonary arterial hypertension (PAH) is a poor prognostic condition in children. We investigated the involvement and the impact of endothelium-derived hyerpolarizing factor (EDHF) in the pathological progression. EDHF-dependent vasodilation in PAH rat induced by monocrotaline or hypoxia was significantly lower than in control rats. The expression of KCa3.1 and KCa2.3 of endothelial cells and KCa1.1 of smooth muscle cells were significantly reduced. These data suggest that EDHF-dependent pulmonary vasodilation is suppressed in PAH. Futhermore, the signal transduction of EDHF would have great impact on the treatment of PAH.
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Report
(4 results)
Research Products
(61 results)