Project/Area Number |
24790770
|
Research Category |
Grant-in-Aid for Young Scientists (B)
|
Allocation Type | Multi-year Fund |
Research Field |
Circulatory organs internal medicine
|
Research Institution | Kumamoto University |
Principal Investigator |
|
Project Period (FY) |
2012-04-01 – 2014-03-31
|
Project Status |
Completed (Fiscal Year 2013)
|
Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2012: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
|
Keywords | 循環器学 / 血管内皮機能 / 血管内皮機能障害 / 慢性腎臓病 / 心拡張不全 / 高血圧 / 食塩感受性 / 一酸化窒素合成酵素 |
Research Abstract |
In the present study, we demonstrated the crucial role of eNOS uncoupling-induced vascular endothelial dysfunction in chronic kidney disease (CKD) and salt-sensitive hypertension using Dahl salt-sensitive hypertensive (DS) rats and eNOS knockout mice. Furthermore, in clinical study, we found that peripheral endothelial dysfunction, assessed by digital peripheral arterial tonometry, was significantly impaired in human cardiac diastolic heart failure (DHF) patients. Furthermore, blood BH4 levels tended to be decreased in DHF patients, indicating the involvement of eNOS uncoupling by BH4 downregulation in human DHF as well as DS rats.
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