Enhanced expression of epithelial sodium channels causes salt‐induced hypertension in mice through inhibition of the α2‐isoform of Na+, K+‐ATPase

Physiological Reports

Frans H. H. Leenen¹  Xiaohong Hou¹  Hong-Wei Wang¹ 

[1] University of Ottawa Heart Institute, Ottawa, Ontario, Canada

关键词: Angiotensin II;    brain;    endogenous ouabain;    Liddle syndrome;   

DOI  :  10.14814/phy2.12383

来源: Wiley

【 摘 要 】

Knockout of the Nedd4-2 gene in mice results in overexpression of epithelial sodium channels (ENaC) on the plasma membrane in the kidney, choroid plexus and brain nuclei. These mice exhibit enhanced pressor responses to CSF [Na⁺] as well as dietary salt-induced hypertension which both can be blocked by central infusion of the ENaC blocker benzamil. Functional studies suggest that ENaC activation in the CNS results in release of endogenous ouabain (EO) and inhibition of the α₂-isoform of Na⁺, K⁺-ATPase. To test this concept more specifically, we studied Nedd4-2^−/− mice expressing the ouabain-resistant

【 授权许可】

CC BY   
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