The Role of Na-K-Activated Adenosine Triphosphatase in Potassium Adaptation. STIMULATION OF ENZYMATIC ACTIVITY BY POTASSIUM LOADING

Patricio Silva; John P. Hayslett; Franklin H. Epstein

doi:10.1172/JCI107460

^{Yale University School of Medicine, New Haven, Connecticut 06510}

^{Harvard Medical Unite, Thorndike Memorial Laboratory, Boston City Hospital, Boston, Massachusetts 02118}

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^{Yale University School of Medicine, New Haven, Connecticut 06510}

^{Harvard Medical Unite, Thorndike Memorial Laboratory, Boston City Hospital, Boston, Massachusetts 02118}

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^{Yale University School of Medicine, New Haven, Connecticut 06510}

^{Harvard Medical Unite, Thorndike Memorial Laboratory, Boston City Hospital, Boston, Massachusetts 02118}

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Published in Volume 52, Issue 11 on November 1, 1973
J Clin Invest. 1973;52(11):2665–2671. https://doi.org/10.1172/JCI107460.
© 1973 The American Society for Clinical Investigation

Published November 1, 1973 - Version history

The specific activity of sodium-potassium-activated adenosine triphosphatase (Na-K-ATPase) in homogenates of rat kidneys increases when the dietary intake of potassium is chronically increased. The effect is seen first and is most prominent in the outer medulla, but large loads of potassium elicit an increase in the cortex as well. Levels of Na-K-ATPase in brian, liver, and muscle, by contrast, are unaffected by potassium loading. Although the changes in enzyme activity in the kidney resemble those reportedly produced by aldosterone, they are not induced by experimental sodium deprivation, and they can be evoked by potassium loading in the absence of the adrenal glands. The results suggest that Na-K-ATPase of renal tubular cells, presumably in the distal tubules and collecting ducts, plays an important role in the phenomenon of potassium adaptation and in the process by which potassium is excreted into the urine.