2022 Fiscal Year Final Research Report
The loss of retinal ganglion cells after administration of aldosterone and development of neuroprotective therapy
Project/Area Number |
20K09827
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Review Section |
Basic Section 56060:Ophthalmology-related
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Research Institution | Hiroshima University |
Principal Investigator |
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Project Period (FY) |
2020-04-01 – 2023-03-31
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Keywords | 緑内障 / アルドステロン / ミネラロコルチコイド受容体 / 神経保護 |
Outline of Final Research Achievements |
Aldosterone was administered systemically in Sprague-Dawley rats. The rats were free access to saline (0.9% NaCl) or water. Eplerenone, mineralocorticoid receptor (MR) antagonist, and hydralazine, vasodilator, were used to determine the effect of antihypertensive drugs on retinal ganglion cell (RGC) loss. Blood pressure was significantly increased in saline intake with or without aldosterone. RGC was significantly decreased in aldosterone treated rats. However, blood pressure did nor affect the RGC loss. Administration of eplerenone or hydralazine in aldosterone treated rat with water instead saline significantly reduced blood pressure. The number of RGC (cells/mm2) was 1868±177 and 1554±34 with eplerenone and hydralazine treated rats, respectively. The RGC loss observed in experimental aldosterone hypertension rat was blood pressure independent loss. Furthermore, MR antagonist has neuroprotective effects independent of IOP or blood pressure.
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Free Research Field |
緑内障
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Academic Significance and Societal Importance of the Research Achievements |
血漿アルドステロン濃度が高いと血圧や眼圧に依存せずに、網膜神経節細胞死をもたらすことが明らかとなった。またこの結果を支持する結果として、血管拡張薬で血圧を下げても網膜神経節細胞死には影響を及ぼさないが、アルドステロンのミネラロコルチコイド受容体に対する作用を抑える薬剤であるミネラロコルチコイド受容体拮抗薬で血圧を下げると網膜神経節細胞死は抑制された。
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