Elucidation of the dysfunctional mechanisms of retinal circulation in the rat models of glaucoma and exploration of novel therapeutic drugs for glaucoma.
Project/Area Number |
22790260
|
Research Category |
Grant-in-Aid for Young Scientists (B)
|
Allocation Type | Single-year Grants |
Research Field |
General pharmacology
|
Research Institution | Kitasato University |
Principal Investigator |
MORI Asami 北里大学, 薬学部, 助教 (80453504)
|
Project Period (FY) |
2010 – 2011
|
Project Status |
Completed (Fiscal Year 2011)
|
Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2011: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2010: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
|
Keywords | 薬理学 / 微小循環 / 緑内障 / 血管生物学 / 網膜 |
Research Abstract |
I revealed that vasodilator responsesof retinal blood vesselsmediated through the mechanism via activation ofendothelial cells, but not those to direct stimulation of smooth muscle, was attenuated in the rat models of glaucoma, which was inducedby retinal ischemia-reperfusionorintravitreal injection of N-methyl-D-aspartic acid. These results suggested that abrormal retinal circulation in glaucoma may accelerateretinal degeneration. It was also suggested that endothelin-1 played an important role to induce severe constriction of theretinal vasculature in the ischemia-reperfusion model. Anagonist of prostanoid EP2 receptor dilatedretinal bloodvessels in the glaucoma model rats, as in the normal rats and inhibited the retinal nerve injury. These results suggestthat prostanoid EP2 receptor agonistsmay be novel candidate drugsfor prevention and/or treatment of glaucoma.
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Report
(3 results)
Research Products
(11 results)