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Am J Physiol Renal Physiol 278: F425-F433, 2000;
0363-6127/00 $5.00
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Vol. 278, Issue 3, F425-F433, March 2000

Mechanisms of inactivation of the action of aldosterone on collecting duct by TGF-beta

Russell F. Husted, Rita D. Sigmund, and John B. Stokes

Department of Internal Medicine, University of Iowa, and Department of Veterans Affairs Medical Center, Iowa City, Iowa 52242

The purpose of these experiments was to investigate the mechanisms whereby transforming growth factor-beta (TGF-beta ) antagonizes the action of adrenocorticoid hormones on Na+ transport by the rat inner medullary collecting duct in primary culture. Steroid hormones 1) increased Na+ transport by three- to fourfold, 2) increased the maximum capacity of the Na+-K+ pump by 30-50%, 3) increased the steady-state levels of the alpha 1-subunit of the Na+-K+-ATPase by ~30%, and 4) increased the steady-state levels of the alpha -subunit of the rat epithelial Na+ channel (alpha -rENaC) by nearly fourfold. TGF-beta blocked the effects of steroids on the increase in Na+ transport and the stimulation of the Na+-K+-ATPase and pump capacity. However, there was no effect of TGF-beta on the steroid-induced increase in mRNA levels of alpha -rENaC. The effects of TGF-beta were not secondary to the decrease in Na+ transport per se, inasmuch as benzamil inhibited the increase in Na+ transport but did not block the increase in pump capacity or Na+-K+-ATPase mRNA. The results indicate that TGF-beta does not inactivate the steroid receptor or its translocation to the nucleus. Rather, they indicate complex pathways involving interruption of the enhancement of pump activity and activation/inactivation of pathways distal to the steroid-induced increase in the transcription of alpha -rENaC.

sodium transport; inner medullary collecting duct; epithelial sodium channel; sodium-potassium-adenosinetriphosphatase; benzamil; glucocorticoid; mineralocorticoid; Northern blot; ribonuclease protection assay; electrophysiology


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