The role of glucocorticoid in renal tubules modulating diurnal change in blood pressure
| Project/Area Number |
17K16075
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Kidney internal medicine
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| Research Institution | The University of Tokyo |
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Principal Investigator |
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| Project Period (FY) |
2017-04-01 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2018: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2017: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 血圧 / 日内変動 / 糖質コルチコイド / ナトリウム輸送体 / 血圧日内変動 / 糖質コルチコイド受容体 / 食塩感受性高血圧 / 鉱質コルチコイド受容体 / 高血圧 |
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| Outline of Final Research Achievements |
The lack of nocturnal drop in blood pressure is one of the risk factors for cardiovascular events. One of the mechanism is the insufficient suppression of corticosteroids in nocturnal period. We found through the observation of mice models, that the rise in corticosterone levels, even within the range of physiological change, causes the dysregulation of several clock genes in the kidneys, and the increase in the gene expression of sodium transporters in distal renal tubules. As a result, corticosterone can induce the increase in the expression and the activity of sodium transporters, followed by the rise in blood pressure in inactivate periods. In addition, corticosterone activate sodium transporters not only through mineralocorticoid receptor, but through glucocorticoid receptor in renal tubules.
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| Academic Significance and Societal Importance of the Research Achievements |
夜間睡眠時には通常血圧が低下するが、この夜間血圧低下が減弱すると心臓病や脳血管障害発症につながると考えられている。この原因の一つとしてストレスホルモンの一種コルチゾールの低下不良が想定されているが、このコルチゾールが日中と同程度まで上昇するだけで血圧上昇を引き起こしうることを見出した。またこの機序として腎臓での食塩再吸収異常が起こることを示し、さらに新しい分子の関与が明らかになった。今回の知見は夜間血圧低下不良に対するあらたな治療アプローチの開発に貢献できると考えられる。
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Report
(3 results)
Research Products
(3 results)
