HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 291/1/F107    most recent 00159.2005v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (1) Citing Articles via Google Scholar Google Scholar Articles by Cao, X. R. Articles by Yang, B. Search for Related Content PubMed PubMed Citation Articles by Cao, X. R. Articles by Yang, B.

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

This article has been cited by other articles:

				P. P. Shi, X. R. Cao, E. M. Sweezer, T. S. Kinney, N. R. Williams, R. F. Husted, R. Nair, R. M. Weiss, R. A. Williamson, C. D. Sigmund, et al. Salt-sensitive hypertension and cardiac hypertrophy in mice deficient in the ubiquitin ligase Nedd4-2 Am J Physiol Renal Physiol, August 1, 2008; 295(2): F462 - F470. [Abstract] [Full Text] [PDF]

				J Manolopoulou, M Bielohuby, S J Caton, C E Gomez-Sanchez, I Renner-Mueller, E Wolf, U D Lichtenauer, F Beuschlein, A Hoeflich, and M Bidlingmaier A highly sensitive immunofluorometric assay for the measurement of aldosterone in small sample volumes: validation in mouse serum J. Endocrinol., February 1, 2008; 196(2): 215 - 224. [Abstract] [Full Text] [PDF]

				P. P. Shi, X. R. Cao, J. Qu, K. A. Volk, P. Kirby, R. A. Williamson, J. B. Stokes, and B. Yang Nephrogenic diabetes insipidus in mice caused by deleting COOH-terminal tail of aquaporin-2 Am J Physiol Renal Physiol, May 1, 2007; 292(5): F1334 - F1344. [Abstract] [Full Text] [PDF]