AJP - Renal Physiology, Vol 266, Issue 4 536-F542, Copyright © 1994 by American Physiological Society

ARTICLES

Na pump defects in chronic uremia cannot be attributed to changes in Na-K-ATPase mRNA or protein

S. Greiber, B. K. England, S. R. Price, R. M. Medford, R. G. Ebb and W. E. Mitch
Renal Division, Emory University School of Medicine, Atlanta, Georgia 30322.

We have found abnormalities in Na-K-adenosine-triphosphatase (Na-K-ATPase) function in different tissues of rats with chronic renal failure (CRF). A potential mechanism for these findings is a change in Na-K-ATPase alpha- and/or beta-gene expression. To evaluate this possibility, we compared CRF with pair-fed, sham-operated rats to determine whether chronic uremia changes the expression of Na-K-ATPase alpha 1-, alpha 2-, beta 1-, and beta 2-isoform mRNAs or protein in different types of skeletal muscle, heart, liver, adipose, and kidney tissue. In CRF rats, alpha 1-mRNA in heart tended to be higher and beta 2-mRNA was lower in fat and kidney. There were no other statistically significant differences in isoform mRNAs in tissues of CRF compared with the control rats. Western blot analysis revealed a 38% increase in alpha 1-protein in adipocytes and a 61% decrease in kidney of CRF rats but no significant differences in the amounts of isoform protein in other tissues. Thus, in uremia, posttranslational events or inhibitors of the enzyme are more likely causes of defects in Na-K-ATPase than changes in mRNA or protein abundance.

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