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NDT Advance Access published online on February 17, 2007
Nephrology Dialysis Transplantation, doi:10.1093/ndt/gfm010
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© The Author [2007]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

WNK4, as thiazides, shuts off NaCl reabsorption to stimulate Na/K exchange*

Francois Verrey

Institute of Physiology and Centre for Integrative Human Physiology (ZIHP), University of Zürich, Winterthurerstrasse 190, CH-8057 Zürich, Switzerland

Correspondence and offprint requests to: François Verrey, Institute of Physiology, University of Zürich, Winterthurerstrasse 190, CH-8057 Zürich, Switzerland. Email: verrey@access.unizh.ch

Keywords: aldosterone; arterial blood pressure; distal convoluted tubule; Familial hyperkalemic hypertension; Gordon's syndrome; K+ secretion; NaCl reabsorption; thiazides

The first 150 words of the full text of this article appear below.

In a manuscript recently published in Nature Genetics, Lalioti et al. [1] show that Wnk4 switches distal nephron function from NaCl reabsorption to Na+/K+ exchange, mainly by dismantling the Na–Cl cotransporter expressing distal convoluted tubule segment DCT1. Interestingly, the structural integrity of this segment had already been shown long ago to depend on Na–Cl cotransporter function, as thiazides provoke similar DCT1 regression as Wnk4 overexpression [2].

The observation underlying the study by Lalioti et al. is that the rare autosomal dominant form of arterial hypertension Familial hyperkalemic hypertension (FHHt), also called Pseudohypoaldosteronism type II (PHAII) or Gordon's Syndrome, is caused by mutations in the gene encoding the protein kinase WNK1 or WNK4 [3]. The salient feature of FHHt is the unusual combination of Na+ and K+ retention. Additional symptoms are hyperchloraemia and metabolic acidosis. The central physiological question that is . . . [Full Text of this Article]



   Transgenic mice expressing wild-type or FHHt mutant Wnk4
 


   Inhibition of NCC by Wnk4 triggers dismantling of the DCT1 nephron segment
 


   Do the other Wnk4 functions described in vitro play a physiological role?
 


   Conclusions
 

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