| Project/Area Number |
17390057
|
|---|
| Research Category |
Grant-in-Aid for Scientific Research (B)
|
| Allocation Type | Single-year Grants |
|---|
| Section | 一般 |
|---|
| Research Field |
General physiology
|
|---|
| Research Institution | Kyoto Prefectural University of Medicine |
|---|
Principal Investigator |
MARUNAKA Yoshinori Kyoto Prefectural University of Medicine, Department of Molecular Cell Physiology, Professor (00127036)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
NIISATO Naomi Kyoto Prefectural University of Medicine, Department of Molecular Cell Physiology, Associate Professor (00237645)
MIYAZAKI Hiroaki Kyoto Prefectural University of Medicine, Department of Molecular Cell Physiology, Associate Professor (30360027)
NAKAJIMA Ken-ichi Kyoto Prefectural University of Medicine, Department of Molecular Cell Physiology, Assistant Professor (40398392)
|
|---|
| Project Period (FY) |
2005 – 2007
|
| Project Status |
Completed (Fiscal Year 2007)
|
| Budget Amount *help |
¥15,480,000 (Direct Cost: ¥14,100,000、Indirect Cost: ¥1,380,000)
Fiscal Year 2007: ¥5,980,000 (Direct Cost: ¥4,600,000、Indirect Cost: ¥1,380,000)
Fiscal Year 2006: ¥4,400,000 (Direct Cost: ¥4,400,000)
Fiscal Year 2005: ¥5,100,000 (Direct Cost: ¥5,100,000)
|
|---|
| Keywords | Epithelial Na Channel / Aldosterone / Hypertension / Renal tubules / Collecting Duct / Intracellular Trafficking / Osmolarity / SGK1 / 高食塩食 / クロライドイオン / JNK / 高食塩 / フラボノイド / ラット |
|---|
| Research Abstract |
The present study has clarified the following points.
In the salt-sensitive hypertensive Dahl rat, ENaC expression was abnormally increased in high salt diet, but not in the salt-resistant hypertensive Dahl rat.
In the salt-sensitive hypertensive Dahl rat, high salt diet abnormally upregulated the expression of SGK1, which regulates the intracellular trafficking of ENaC.
These observations suggest that in the salt-sensitive hypertensive Dahl rat, expression of ENaC and its regulator, SGK1, is abnormally regulated by high salt-diet, resulting in hypertension.
This abnormally upregulation of ENaC expression was partially diminished by a flavonoid, quercetin. Hyposomotic stress elevated the expression of ENaC.
This hyposmotic stress-induced elevation of ENaC expression was mediated via a decrease in the cytosolic chloride ion concentration.
Aldosterone inhibited the endocytosis of ENaC protein.
The aldosterone-induced ENaC proteins were mainly located in ER
p38 was involved in hyposmotic stress-induced upregulation of ENaC expression.
|
