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Author Notes:

Corresponding author: Brandi M. Wynne, Email: bwynne@emory.edu

B.M.W. and R.S.H. conceived manuscript.

B.M.W., A.C.M., O.K. and F.T. performed experiments.

B.M.W. and F.T. prepared figures.

B.M.W. wrote manuscript; B.M.W., D.C.E. and R.S.H. edited manuscript.

All authors approved final copy.

The authors would like to thank Dr. Jan Loffing for providing antibodies.

The authors declare that they have no competing interests.


Research Funding:

This work was supported by the National Institutes of Health R01 DK-085097 (to R.S.H.), T32 DK07656 (B.M.W.), R37 DK037963 (D.C.E.).

Also by the Department of Veteran Affairs MERIT Award I01BX002322-01 (R.S.H.) and Swiss National Foundation (F.T.).

Aldosterone Modulates the Association between NCC and ENaC.


Journal Title:

La Science dans la Republique populaire roumaine


Volume 7, Number 1


, Pages 4149-4149

Type of Work:

Article | Final Publisher PDF


Distal sodium transport is a final step in the regulation of blood pressure. As such, understanding how the two main sodium transport proteins, the thiazide-sensitive sodium chloride cotransporter (NCC) and the epithelial sodium channel (ENaC), are regulated is paramount. Both are expressed in the late distal nephron; however, no evidence has suggested that these two sodium transport proteins interact. Recently, we established that these two sodium transport proteins functionally interact in the second part of the distal nephron (DCT2). Given their co-localization within the DCT2, we hypothesized that NCC and ENaC interactions might be modulated by aldosterone (Aldo). Aldo treatment increased NCC and αENaC colocalization (electron microscopy) and interaction (coimmunoprecipitation). Finally, with co-expression of the Aldo-induced protein serum- and glucocorticoid-inducible kinase 1 (SGK1), NCC and αENaC interactions were increased. These data demonstrate that Aldo promotes increased interaction of NCC and ENaC, within the DCT2 revealing a novel method of regulation for distal sodium reabsorption.

Copyright information:

© The Author(s) 2017

This is an Open Access work distributed under the terms of the Creative Commons Attribution 4.0 International License (https://creativecommons.org/licenses/by/4.0/).
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