Abnormal cation transport in uremia. Mechanisms in adipocytes and skeletal muscle from uremic rats.

W Druml; R A Kelly; R C May; W E Mitch

doi:10.1172/JCI113435

Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts 02115.

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Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts 02115.

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Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts 02115.

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Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts 02115.

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Published in Volume 81, Issue 4 on April 1, 1988
J Clin Invest. 1988;81(4):1197–1203. https://doi.org/10.1172/JCI113435.
© 1988 The American Society for Clinical Investigation

Published April 1, 1988 - Version history

The cause of the abnormal active cation transport in erythrocytes of some uremic patients is unknown. In isolated adipocytes and skeletal muscle from chronically uremic chronic renal failure rats, basal sodium pump activity was decreased by 36 and 30%, and intracellular sodium was increased by 90 and 50%, respectively, compared with pair-fed control rats; insulin-stimulated sodium pump activity was preserved in both tissues. Lower basal NaK-ATPase activity in adipocytes was due to a proportionate decline in [3H]ouabain binding, while in muscle, [3H]ouabain binding was not changed, indicating that the NaK-ATPase turnover rate was decreased. Normal muscle, but not normal adipocytes, acquired defective Na pump activity when incubated in uremic sera. Thus, the mechanism for defective active cation transport in CRF is multifactorial and tissue specific. Sodium-dependent amino acid transport in adipocytes closely paralleled diminished Na pump activity (r = 0.91), indicating the importance of this defect to abnormal cellular metabolism in uremia.