The significance of endothelin-1 and its receptors on nitric oxide production
Project/Area Number |
23590314
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
General pharmacology
|
Research Institution | Osaka University of Pharmaceutical Sciences |
Principal Investigator |
OHKITA MAMORU 大阪薬科大学, 薬学部, 准教授 (60449824)
|
Co-Investigator(Kenkyū-buntansha) |
MATSUMURA Yasuo 大阪薬科大学, 薬学部, 教授 (40140230)
|
Project Period (FY) |
2011 – 2013
|
Project Status |
Completed (Fiscal Year 2013)
|
Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2012: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2011: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
|
Keywords | エンドセリン / 一酸化窒素 / ETB受容体 / 内皮細胞 |
Research Abstract |
There was no difference in NO production under basal condition between homozygous ETB deficient and wild-type rats. However, NOx output in the renal tissue by continuous infusion of L-arginine was significantly lower in homozygous than wild-type rats. This reduced converting activity of L-arginine to NO in homozygous rats was completely recovered by the acute administration of a selective ETA receptor antagonist. These results suggest that the augmentation of ET-1/ETA receptor-mediated actions involves in the decline of renal NO production under ETB receptor dysfunction. On the other hand, serum NOx levels in L-arginine treated homozygous rats were significantly increased compared to that of wild type rats, and that the expression of relative factors in NO production also significantly increased in the aortic tissue, suggesting that different mechanisms would control NO production in kidney and vasculature of homozygous rats, respectively.
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Report
(4 results)
Research Products
(9 results)