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Both mineralo- and glucocorticoids stimulate renal Na-K-ATPase, but their relative role in the regulation of the enzyme remains controversial. In this study we measured Na-K-ATPase activity in the cortical collecting tubule (CCT) of adrenalectomized rats replaced with either the native mineralocorticoid (aldosterone) or glucocorticoid (corticosterone) in doses calculated to yield previously determined physiologic concentrations of these hormones (5 ng X dl-1 and 5 micrograms X dl-1, respectively). This was achieved by continuous delivery of aldosterone (1 microgram X 100 g-1 X d-1) from an osmotic minipump or of corticosterone (2 pellets of 20 mg each), implanted subcutaneously either at adrenalectomy or 7 d later, when Na-K-ATPase activity reached its nadir. Adrenalectomized rats not receiving hormone replacement and adrenal-intact animals served as controls. The CCT was chosen because it contains the highest concentration of binding sites for both hormones. Na-K-ATPase activity declined 52% in the CCT of untreated adrenalectomized rats after 7 d, and remained unchanged thereafter. Physiologic replacement doses of aldosterone prevented this decline and restored the activity of the enzyme after it had been allowed to decrease maximally following adrenal ablation, whereas similar replacement of corticosterone was without effect. These observations suggest that under physiologic conditions Na-K-ATPase in the CCT, a probable target nephron segment of both hormones, is under mineralocorticoid rather than glucocorticoid control.

Regulation of renal Na-K-ATPase in the rat. Role of the natural mineralo- and glucocorticoid hormones.