PubMed 11562398
Referenced in: none
Automatically associated channels: Kv7.1 , Slo1
Title: Role of KCNE1-dependent K+ fluxes in mouse proximal tubule.
Authors: V Vallon, F Grahammer, K Richter, M Bleich, F Lang, J Barhanin, H Völkl, R Warth
Journal, date & volume: J. Am. Soc. Nephrol., 2001 Oct , 12, 2003-11
PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/11562398
Abstract
The electrochemical gradient for K+ across the luminal membrane of the proximal tubule favors K+ fluxes to the lumen. Here it was demonstrated by immunohistochemistry that KCNE1 and KCNQ1, which form together the slowly activated component of the delayed rectifying K+ current in the heart, also colocalize in the luminal membrane of proximal tubule in mouse kidney. Micropuncture experiments revealed a reduced K+ concentration in late proximal and early distal tubular fluid as well as a reduced K+ delivery to these sites in KCNE1 knockout (-/-), compared with wild-type (+/+) mice. These observations would be consistent with KCNE1-dependent K+ fluxes to the lumen in proximal tubule. Electrophysiological studies in isolated perfused proximal tubules indicated that this K+ flux is essential to counteract membrane depolarization due to electrogenic Na+-coupled transport of glucose or amino acids. Clearance studies revealed an enhanced fractional urinary excretion of fluid, Na+, Cl-, and glucose in KCNE1 -/- compared with KCNE1 +/+ mice that may relate to an attenuated transport in proximal tubule and contribute to volume depletion in these mice, as indicated by higher hematocrit values.