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2019 Fiscal Year Final Research Report

How does potassium regulate blood pressure through sodium-transporter?

Research Project

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Project/Area Number 18K15995
Research Category

Grant-in-Aid for Early-Career Scientists

Allocation TypeMulti-year Fund
Review Section Basic Section 53040:Nephrology-related
Research InstitutionTokyo Medical and Dental University

Principal Investigator

Nomura Naohiro  東京医科歯科大学, 大学院医歯学総合研究科, 非常勤講師 (50735800)

Project Period (FY) 2018-04-01 – 2020-03-31
Keywords血圧 / 電解質 / バーター症候群 / ギッテルマン 症候群 / カルシニューリン阻害剤
Outline of Final Research Achievements

High potassium (K) intake decreases hypertension and associated lower mortality. On the other hand, hyperkalemia causes sudden death with fatal cardiac arrhythmia and is also related to higher mortality.
Renal sodium (Na)-chloride (Cl) cotransporter (NCC), expressed in the distal convoluted tubule, is a key molecule in regulating urinary K excretion. K intake affects the activity of the NCC, which is related to salt-sensitive hypertension. NCC is known to be regulated by WNK-SPAK signal cascade. We discovered that the suppression of NCC by K loading was regulated by another mechanism. We found that calcium signal through sodium-calcium exchanger (NCX) stimulates calcineurin, which dephosphorylates NCC. This finding could lead to novel treatment against Gitelman syndrome, which is caused by loss of function of NCC.

Free Research Field

腎臓内科学

Academic Significance and Societal Importance of the Research Achievements

ナトリウムクロライド共輸送体は、腎臓においてナトリウムやカリウムのバランスをとるために主要な役割を担っており、この輸送体のメカニズムを明らかとすることは、血圧管理・体内の水分・電解質バランス調整に役立つと考えられる。
また、ナトリウム輸送体の機能障害が原因であるギッテルマン 症候群やバーター症候群の発症にも関わっており、これらの疾患の治療につながる可能性がある。

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Published: 2021-02-19  

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