Dissociation of Na-K-ATPase specific activity and net reabsorption of sodium.
Prevoius studies have suggested that the increase in specific activity of Na-K-ATPase in renal tissue during treatment with glucocorticoids occurred as a result of aconcurrent rise in net tubular reabsorption of sodium.  Since recent data have indicated a specific effect of glucocortiocoids on epithelial cells, experiments were performed to determine whether enzyme activity and net sodium reabsorption could be dissociated. Evidence is provided demonstrating that base-line specific activity of Na-K-ATPase in rat renal cortex and outer medulla does not correlate directly with net sodium reabsorption since enzyme activity did not change after a chronic reduction in glomerularfiltration rate and the rate of sodium reabsorption.  Further studies showed a markedrise in Na-K-ATPase after 4 days of treatment with methylprednisolone despite a fall in sodium absorption.  These results suggest a direct effect of glucocorticoids onrenal Na-K-ATPase and illistrate the difficulty in assigning a transport role tothis enzyme from the correlation of specific activity with rates of net electrolyte transport.
D000251:Adenosine Triphosphatases / Q000378:metabolism*; D000818:Animals; D001692:Biological Transport; D005919:Glomerular Filtration Rate; D005938:Glucocorticoids / Q000494:pharmacology*; D007672:Kidney Cortex / Q000378:metabolism; D007679:Kidney Medulla / Q000378:metabolism; D007684:Kidney Tubules / Q000378:metabolism*; D008775:Methylprednisolone / Q000494:pharmacology; D011188:Potassium; D051381:Rats; D012964:Sodium / Q000378:metabolism*; D013268:Stimulation, Chemical
D005938:Glucocorticoids; D012964:Sodium; D000251:Adenosine Triphosphatases; D011188:Potassium; D008775:Methylprednisolone