Glucocorticoid Regulation of Prolactin Receptors in Kidneys and Adrenals of Male Rats*

Abstract

Binding of PRL [prolactin] to specific binding sites in kidney and adrenal was time- and temperature-dependent. The binding of [125I]iodo-PRL to kidney preparations increased with increasing amounts of membrane protein. Adrenalectomy increased concentrations of PRL receptors in the kidneys 49% above control values, whereas dexamethasone treatment reduced PRL receptors to below control levels. The latter effect was not mediated primarily through the pituitary because dexamethasone treatment of hypophysectomized rats also produced a significant decrease in specific receptor-binding from 2.85 .+-. 0.20%-0.74 .+-. 0.08%. However, the pituitary was partly responsible for maintaining PRL receptors because kidney membrane preparations from intact control rats specifically bound 9.98 .+-. 0.32% ovine [125I]iodo-PRL after incubation, which is significantly higher than what was found in hypophysectomized rats. In the adrenals, a reduction in specific PRL binding also was observed after hypophysectomy, from 12.72 .+-. 0.63%-5.73 .+-. 0.33%, and this was decreased further to 3.18 .+-. 0.45% after dexamethasone treatment. Hydrocortisone as well as dexamethasone were effective in lowering PRL receptor binding in kidney membrane preparations in intact male rats, and this effect was found to be dose-dependent by using a high and low dose of dexamethasone. A low dose of dexamethasone also produced a progressive reduction in PRL-binding activity in the kidney after 5, 10 and 20 days of treatment, with receptor values decreasing from 3.95 .+-. 0.27%, -1.94 .+-. 0.33% and 1.52 .+-. 0.13%, respectively. Scatchard analysis of kidney membrane preparations indicated that changes in specific binding were due to binding capacity rather than Kd changes. Neither aldosterone, its antagonist, spieonolactone, nor renin was effective in altering concentrations of PRL receptors in the kidneys or adrenals of intact rats, suggesting that mineralocorticoids have little, if any, effect on PRL receptors in these tissues. The adrenal glucocorticoids are important regulators of PRL receptors in the kidneys and adrenals of male rats.