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Renal defects in KCNE1 knockout mice are mimicked by chromanol 293B in vivo : identification of a KCNE1‐regulated K + conductance in the proximal tubule
Author(s) -
Neal A. M.,
Taylor H. C.,
Millar I. D.,
Kibble J. D.,
White S. J.,
Robson L.
Publication year - 2011
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2011.209155
Subject(s) - knockout mouse , kidney , endocrinology , medicine , chemistry , wild type , in vivo , potassium channel , voltage clamp , biology , biophysics , electrophysiology , biochemistry , mutant , receptor , microbiology and biotechnology , gene
Non‐technical summary The kidney plays a critical role in regulating body fluid volume and blood pressure by conserving ions, solutes and water. Knowing the processes that underpin the handling of ions, solutes and water by the kidney is essential to our understanding of fluid and blood pressure regulation. Movement of ions is mediated by specific transport proteins found in the membranes of kidney cells. These proteins are regulated by additional proteins, called accessory proteins. In the current study, we have examined the role of the accessory protein KCNE1 in regulating a channel, KCNQ1, which is important in kidney function. We have observed that in the absence of KCNE1 the kidney has difficulty conserving sodium, chloride and water. However, by using specific inhibitors of these proteins we have also determined that although KCNE1 has a role in kidney function, the mechanism of its action is unlikely to be by regulating the protein KCNQ1.