Abstract
In a companion paper we reported a large increment in Na+-K+-ATPase activity and [3H]ouabain binding in the inner stripe of outer medullary collecting tubules from K-depleted rats. To test the hypothesis that the increased number of Na+-K+ pumps in these animals may be involved in potassium reabsorption we examined the effect of ouabain on K excretion by isolated, perfused kidneys from rats fed a K-free diet for 3 wk. Kidneys from K-depleted rats retain potassium avidly, both the fractional (FEK) and absolute K excretion being approximately fivefold lower than in control kidneys. Ouabain (5 mM) increased FEK in kidneys from each K-depleted rat [mean from 8.5 to 34.4%, P less than 0.001, at average (4.5 mM) perfusate K]; similar results were obtained when kidneys were perfused with low (approximately 2 mM) and high (greater than or equal to 8 mM) potassium concentrations. In contrast, ouabain produced a variable effect in control kidneys, that depended on the perfusate potassium concentration. In K-depleted rats amiloride (10(-4) M) did not significantly alter K excretion and did not block the ouabain-induced kaliuresis, suggesting that the latter is not due to enhanced secretion secondary to increased distal fluid delivery. These results provide evidence for ouabain-sensitive potassium reabsorption in kidneys of chronically K-depleted rats, and suggest an explanation for the increased Na+-K+-ATPase observed in such animals.
Publisher
American Physiological Society
Cited by
16 articles.
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