Urokinase-type plasminogen activator (uPA) is not essential for epithelial sodium channel (ENaC)-mediated sodium retention in experimental nephrotic syndrome.

Bernhard N Bohnert,Sophie Daiminger,Matthias Wörn,Florian Sure,Tobias Staudner,Alexandr V Ilyaskin, Firas Batbouta,Andrea Janessa,Jonas C Schneider,Daniel Essigke,Sandip Kanse,Silke Haerteis,Christoph Korbmacher,Ferruh Artunc

Acta physiologica (Oxford, England)（2019）

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摘要

uPA is responsible for the conversion of aberrantly filtered plasminogen to plasmin in the tubular lumen in vivo. However, uPA dependent plasmin generation is not required for ENaC-mediated sodium retention in experimental nephrotic syndrome. This article is protected by copyright. All rights reserved.

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关键词

amiloride - epithelial sodium channel (ENaC) - urokinase-type plasminogen activator ,plasminogen - nephrotic syndrome ,sodium retention

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