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Mice heterozygous for β-ENaC deletion have defective potassium excretion
Journal article   Peer reviewed

Mice heterozygous for β-ENaC deletion have defective potassium excretion

X Renee Cao, P. Peter Shi, Rita D. Sigmund, Russell F. Husted, Curt D. Sigmund, Roger A. Williamson, John B. Stokes and Baoli Yang
American Journal of Physiology-Renal Physiology, Vol.291(1), pp.F107-F115
07/01/2006
DOI: 10.1152/ajprenal.00159.2005
PMCID: PMC2818793
PMID: 16571596
url
http://doi.org/10.1152/ajprenal.00159.2005View
Open Access

Abstract

The present studies were designed to determine whether mice heterozygous for deletion of β-ENaC exhibited defects in Na+/K+ transport and blood pressure regulation. In response to an acute KCl infusion, +/− mice developed higher serum [K+] and excreted only 40% of the K+ excreted by +/+ mice. After 6 days on a low (0.01%)-Na+ diet, the cumulative Na+ excretion from days 3-6 was greater for +/− mice. This low-Na+ diet caused higher serum [K+] and lower K+ excretion rates in +/− mice than in +/+ mice, but the rectal potential differences were not different. Analyses of mRNA from mice on this diet showed the expected ∼50% reduction of β-ENaC in kidney and colon of +/− mice. Unexpectedly, the level of γ-ENaC mRNA was similarly reduced. NHE3 mRNA was ∼30% higher in +/− mice whereas mRNA of the Na-K-2Cl cotransporter was not different. Also unexpectedly, the amount of β-ENaC proteins was similar in both groups of mice but there was a reduction of one form of γ-ENaC in +/− mice. These experiments demonstrate that mice heterozygous for β-ENaC have a small but detectable defect in their ability to conserve Na+ and a more readily apparent defect in the ability to secrete K+.
 Obstetrics and Gynecology

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