Glucocorticoid effects on Na-K-ATPase in rabbit nephron segments

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Abstract
The effect of dexamethasone on Na-K-ATPase activity in 6 nephron segments of the adrenalectomized rabbit was determined. Treatment consisted of 1.4 .mu.g dexamethasone .cntdot. 100 g/body wt .cntdot. day for 7 days prior to the study of the nephron segments. Enzyme activity was determined in individual nephron segments by a microfluorometric assay. There was 40-50% less activity of Na-K-ATPase in the S1 portion of the proximal convoluted tubule (PCT, S1), the medullary thick ascending limb (MTAL) and the distal convoluted tubule (DCT) of adrenalectomized rabbits compared with that of control (sham-operated) animals. There was no significant difference in the enzyme activity in proximal straight tubules (PST, S2 and S3) and cortical thick ascending limb (CTAL) of adrenalectomized and control animals. Dexamethasone treatment produced a dexamethasone concentration of 5 .+-. 0.8 nM in the plasma and increased Na-K-ATPase activity in PCT (S1), MTAL and DCT of the adrenalectomized animals to the control levels without significantly affecting the enyzme activity in the PST (S2, S3) or CTAL. The concentration of dexamethasone in the plasma was such that the hormone should bind mainly to dexamethasone receptors (Kd = 5 nM) and very little to aldosterone receptors (Kd > 60 nM). Glucocorticoids probably stimulate Na-K-ATPase in PCT, MTAL and DCT through glucocorticoid (Type II) receptors and not through mineralocorticoid (Type I) receptors.