Mice heterozygous for β-ENaC deletion have defective potassium excretion

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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+.