Role of medullary Na-K-ATPase in renal potassium adaption.
Since recent studies have shown that chronic potassium loading stimulates the specific activity of Na-K-ATPase in renal tissue, experiments were performed to determine whether increased enzyme acitivity correlated with renal adaptation for accelerated potassium excretion. The Na-K-ATPase activity in different renal zones was correlated with the maximum rate of potassium excretion during the intravenous infusion of KCl in animals with normal and reduced renal function, animals on a varied potassium diet and animals treated with methylprednisolone or deoxycorticosterone acetate. The enhanced ability to excrete a potassium load was associated with increased enzyme activity in the outer or red medulla, whether the change in Na-K-ATPase was caused by chronic potassium loading, methylprednisolone treatment, or partial nephrectomy. There was no evidence that a rise in enzyme activity in the cortex influenced the rate of potassium secretion. Moreover, stimulation of Na-K-ATPase in the inner medulla-papilla did not augment the rate of potassium excretion above that found in animals with an increase in enzyme in the outer medulla alone. These experiments provide evidence that links Na-K-ATPase to the mechanism of renal potassium adaptation and suggest that the major increment in potassium secretion by the adapted kidney occurs in the outer medulla.
D000251:Adenosine Triphosphatases / Q000378:metabolism*; D000818:Animals; D003900:Desoxycorticosterone / Q000494:pharmacology; D007668:Kidney / Q000201:enzymology* / Q000378:metabolism; D007672:Kidney Cortex / Q000201:enzymology; D007679:Kidney Medulla / Q000201:enzymology*; D008297:Male; D008775:Methylprednisolone / Q000494:pharmacology; D011188:Potassium / Q000378:metabolism*; D011189:Potassium Chloride / Q000494:pharmacology; D051381:Rats
D003900:Desoxycorticosterone; D011189:Potassium Chloride; D000251:Adenosine Triphosphatases; D011188:Potassium; D008775:Methylprednisolone