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Mice heterozygous for beta-ENaC deletion have defective potassium excretion. Am J Physiol Renal Physiol 2006 Jul;291(1):F107-15

Date

03/31/2006

Pubmed ID

16571596

Pubmed Central ID

PMC2818793

DOI

10.1152/ajprenal.00159.2005

Scopus ID

2-s2.0-33745397263 (requires institutional sign-in at Scopus site)   13 Citations

Abstract

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+.

Author List

Cao XR, Shi PP, Sigmund RD, Husted RF, Sigmund CD, Williamson RA, Stokes JB, Yang B

Author

Curt Sigmund PhD Chair, Professor in the Physiology department at Medical College of Wisconsin




MESH terms used to index this publication - Major topics in bold

Aldosterone
Animals
Blood Pressure
Epithelial Sodium Channels
Female
Gene Deletion
Heterozygote
Homeostasis
Kidney
Male
Mice
Mice, Inbred C57BL
Mice, Inbred Strains
Potassium
RNA, Messenger
Sodium
Sodium Channels
Sodium, Dietary
Sodium-Potassium-Chloride Symporters
Sodium-Potassium-Exchanging ATPase