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The present studies were designed to determine whether mice heterozygous for deletion of beta-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 approximately 50% reduction of beta-ENaC in kidney and colon of +/-mice. Unexpectedly, the level of gamma-ENaC mRNA was similarly reduced. NHE3 mRNA was approximately 30% higher in +/-mice whereas mRNA of the Na-K-2Cl cotransporter was not different. Also unexpectedly, the amount of beta-ENaC proteins was similar in both groups of mice but there was a reduction of one form of gamma-ENaC in +/-mice. These experiments demonstrate that mice heterozygous for beta-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+.

Mice heterozygous for β-ENaC deletion have defective potassium excretion