| Project/Area Number |
16K18998
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Multi-year Fund |
|---|
| Research Field |
General physiology
|
|---|
| Research Institution | National Institute for Basic Biology |
|---|
Principal Investigator |
Nomura Kengo 基礎生物学研究所, 統合神経生物学研究部門, 特別協力研究員 (10734519)
|
|---|
| Project Period (FY) |
2016-04-01 – 2018-03-31
|
| Project Status |
Completed (Fiscal Year 2017)
|
| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2017: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
|
|---|
| Keywords | 食塩 / 血圧 / 交感神経 / ナトリウム / ナトリウムチャンネル / 食塩感受性高血圧 / 脳・神経 / イオンチャンネル |
|---|
| Outline of Final Research Achievements |
Salt-sensitive hypertension is characterized by exaggerated increment in blood pressure during high salt intake. Although increment of sodium concentration in body fluids during high salt intake could be involved in the pathogenesis of salt-sensitive hypertension, the mechanism is unknown. I hypothesized that brain sodium sensor Nax senses increased sodium concentration in cerebrospinal fluid, and then elevates blood pressure via activation of sympathetic nervous system. To reveal that Nax is involved in blood pressure regulation, I induced elevation of sodium concentration in body fluids, and compared blood pressure of wild type mice and Nax-knockout mice. In addition, I tried to elucidate the brain mechanisms mediating salt-induced blood pressure elevation. This study could identify the central sodium sensor involved in salt-sensitive hypertension and contribute to the development of the therapeutics through the presentation of a novel drug target.
|
