Mechanism of hypertension in metabolic syndrome: the role of central sympathoexcitation
| Project/Area Number |
24591226
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (C)
|
| Allocation Type | Multi-year Fund |
|---|
| Section | 一般 |
|---|
| Research Field |
Kidney internal medicine
|
|---|
| Research Institution | The University of Tokyo |
|---|
Principal Investigator |
Fujita Megumi 東京大学, 医学部附属病院, 助教 (50447405)
|
|---|
| Project Period (FY) |
2012-04-01 – 2016-03-31
|
| Project Status |
Completed (Fiscal Year 2015)
|
| Budget Amount *help |
¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2014: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
|
|---|
| Keywords | 高血圧 / メタボリックシンドローム / 交感神経活動 / ミネラロコルチコイド受容体 / 酸化ストレス |
|---|
| Outline of Final Research Achievements |
We have shown previously that sympathoexcitation by brain oxidative stress mediates arterial pressure elevation in hypertension, and also shown that aldosterone-mineralocorticoid receptor (MR) activation mediates oxidative stress-induced cardiac and renal dysfunction. Then, we hypothesized that brain MR activation could mediate arterial pressure elevation through brain oxidative stress-induced sympathoexcitation. We used high-salt-loaded Dahl-salt-sensitive rats, high-fat-loaded-Sprague-Dawley rats and Dahl-S.Z-Lepr(fa)/Lepr(fa)). In these rats, mRNA expression of Sgk-1 and PAI-1 in the hypothalamus was significantly enhanced, which suggested MR activation. Moreover, chronic intracerebroventricular eplerenone significantly reduced sympathetic nerve activity and arterial pressure. In conclusion, brain aldosterone-MR activation through btsin oxidative stress-induced sympathoexcitation can be a possible pathogenic background of hypertension in metabolic syndrome.
|
Report
(5 results)
Research Products
(31 results)
