The pituitary regulation of the sexually differentiated PRL receptor in rat liver was studied. PRL receptors were measured in a crude membrane fraction (105,000 x g pellet) using [125I]iodohuman PRL as tracer. Human GH (hGH), continuously administered by Alzet osmotic minipumps with an infusion rate of 5 μg/h for 1 week, was shown to induce PRL receptors in livers from male and female hypophysectomized-gonadectomized rats. The PRL receptors were increased to a level found in control female rat livers. This inductive effect of hGH was also seen in adrenalectomized and thyroidectomized male rats. In intact male rats given hGH, PRL receptors were increased to a female level in 4-7 days. hGH was effective in doses of 2.5 and 5 μg/μl in inducing a female receptor pattern. The induced PRL receptors in male rats had characteristics similar to those of hepatic PRL receptors in female rats when data were calculated according to Scatchard (K(d) = 0.13 x 10-9 vs. 0.15 x 10-9 M; number of binding sites 88 vs. 57 fmol/mg protein). Also, the endogenous rat hormones, rat PRL (rPRL) and rat GH (rGH), were administered by minipumps to hypophysectomized male rats. With the infusion rate used (10 μg/h), rPRL had no effect, whereas rGH (NIAMDD-B6) increased receptor levels to approximately 37% of the female control level. A more complete induction of PRL receptors (75% of the female control levels) in hypophysectomized males was achieved using another preparation of rGH (NIAMDD I-4). Also, in hypophysectomized female rats, rPRL was ineffective in inducing PRL receptors. On the other hand, ovine PRL was found to give a partial restoration of PRL receptors in hypophysectomized female rats. The results indicate that GH or a peptide related to GH may be involved in the regulation of hepatic PRL receptors. However, the results do not rule out the possibility that rPRL, when present in doses other than those used in the present investigation, may also play a role in receptor regulation.
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