AJP - Renal Physiology, Vol 248, Issue 4 487-F491, Copyright © 1985 by American Physiological Society
Glucocorticoid effects on Na-K-ATPase in rabbit nephron segments
L. C. Garg, N. Narang and C. S. Wingo
We determined the effect of dexamethasone on Na-K-ATPase activity in six
nephron segments of the adrenalectomized rabbit. Treatment consisted of 1.4
micrograms dexamethasone X 100 g body wt-1 X day-1 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 enzyme 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 greater than 60 nM). Thus, glucocorticoids
probably stimulate Na-K-ATPase in PCT, MTAL, and DCT through glucocorticoid
(Type II) receptors and not through mineralocorticoid (Type I) receptors.
