| First Author | Cao XR | Year | 2006 |
| Journal | Am J Physiol Renal Physiol | Volume | 291 |
| Issue | 1 | Pages | F107-15 |
| PubMed ID | 16571596 | Mgi Jnum | J:109444 |
| Mgi Id | MGI:3628969 | Doi | 10.1152/ajprenal.00159.2005 |
| Citation | Cao XR, et al. (2006) Mice heterozygous for beta-ENaC deletion have defective potassium excretion. Am J Physiol Renal Physiol 291(1):F107-15 |
| abstractText | 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(+). |
