Regulation of adrenal and testicular prolactin receptors by adrenocorticotropin and luteinizing hormone.

Receptors for PRL in the adrenal, ovary, and testis undergo marked and rapid depletion after trophic stimulation by ACTH and LH, respectively. The mechanism of such heterologous regulation of PRL receptors in the testis and adrenal cortex was further analyzed in hormone-treated male rats. Hormone-stimulated turnover of PRL receptors was not prevented by treatment with cycloheximide (75 and 300 μg), which caused an 80% fall in testicular and adrenal sites within 1 h, followed by a return to normal in 24 h. When steroid secretion was inhibited by treatment with 4-aminopyrazolopyrimidine for 4 days, with a 90% decrease in serum cholesterol, ACTH and LH retained the ability to reduce PRL receptors by 60–70% 12 and 24 h after injection. Similarly, during blockade of steroidogenesis by aminoglutethimide, treatment with 10 U ACTH or 100 μg ovine LH still reduced PRL receptors by about 70%. When adrenal and testicular steroidogeneses were stimulated by the administration of 8-bromo cAMP, serum corticosterone and ...

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