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Mice heterozygous for -ENaC deletion have defective potassium excretion

¹Department of Obstetrics and Gynecology, ²Internal Medicine, ³Physiology and Biophysics, Carver College of Medicine, University of Iowa, and ⁴Veterans Affairs Medical Center, Iowa City, Iowa

Submitted 18 April 2005 ; accepted in final form 4 March 2006

The present studies were designed to determine whether mice heterozygous for deletion of -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 -ENaC in kidney and colon of +/– mice. Unexpectedly, the level of -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 -ENaC proteins was similar in both groups of mice but there was a reduction of one form of -ENaC in +/– mice. These experiments demonstrate that mice heterozygous for -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⁺.

sodium; homeostasis; heterozygote; low-Na⁺ diet

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