Abnormal brain Na handling contributes to salt-induced cardiac dysfunction in heart failure model
| Project/Area Number |
21790730
|
|---|
| Research Category |
Grant-in-Aid for Young Scientists (B)
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
Circulatory organs internal medicine
|
|---|
| Research Institution | Kyushu University |
|---|
Principal Investigator |
ITO Koji Kyushu University, 大学病院, 助教 (10452757)
|
|---|
| Project Period (FY) |
2009 – 2010
|
| Project Status |
Completed (Fiscal Year 2010)
|
| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2010: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2009: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
|
|---|
| Keywords | 心不全 / 食塩 / 脳 / Naチャネル / ミネラルコルチコイド / 交感神経活動 / 食塩摂取 / 心肥大(心不全) / ミネラルコルチコイド受容体 / ナトリウムチャネル |
|---|
| Research Abstract |
In pressure-overload mice, high-salt intake increased 24-h urinary catecholamine excretion resulting in cardiac dysfunction, but not in Sham-mice. We focused mineralocorticoid receptor (MR), as Na channels activator and CYP-epoxyeicoatrienoic acid (EET) pathway, as Na channels inhibitor. We examined the extent/activity of brain MR and Cyp2C9 expression and 11,12-epoxyeicosatrienoic acids (EET) concentration. In Sham-mice, high-salt intake decreased MR activation, but in pressure-overload mice. ICV infusion of MR blocker attenuated the salt-induced sympathetic activation and cardiac dysfunction in pressure-overload mice. In Sham-mice, high-salt intake increased the brain cyp2C9 expression and 11,12-EET concentration but not in pressure-overload mice. These results indicate that, in mice with pressure-overload, high-salt intake increases sympathetic outflow via the activation of brain Na channels through MR activation and insufficient activation of CYP-EET pathway.
|
Report
(3 results)
Research Products
(11 results)
