Induction of lactogenic receptors. I. In the liver of hypophysectomized female rats.
To identify the hormones which affect lactogenic receptors in the liver of chronically hypophysectomized female rats, hormones were injected s.c. for 7 days. Specific binding (%, SB) of labelled ovine prolactin (PRL) in liver membrane preparations (1000,000 X g pellet) of controls was 1%. Estradiol (E2), cortisone (Con), ACTH or bovine growth hormone (bGH) treatment did not induce hepatic binding sites for PRL. Human GH and a single dose of 2mg PRL (but not lower doses) increased SB of PRL. Treatment with oPRL plus ACTH was less effective than hGH plus ACTH (13 vs 28%); combinations of oPRL plus Con as well as administration of oPRL plus ACTH to hypophysectomized and adrenalectomized female rats did not induce SB for PRL. Therapy with oPRL plus hGH (26%) was more potent than oPRL plus bGH (2%). These studies suggest that PRL, GH, and ACTH induce and in concert with sex steroids, modulate the lactogenic receptors in the female rat liver. The effect of ACTH is not due to increased adrenal corticoid secretion.
D000315:Adrenalectomy; D000324:Adrenocorticotropic Hormone / Q000494:pharmacology; D000818:Animals; D002462:Cell Membrane / Q000187:drug effects / Q000378:metabolism; D003348:Cortisone / Q000494:pharmacology; D004958:Estradiol / Q000494:pharmacology; D005260:Female; D013006:Growth Hormone / Q000097:blood / Q000494:pharmacology; D007016:Hypophysectomy; D007700:Kinetics; D008099:Liver / Q000187:drug effects / Q000378:metabolism*; D011388:Prolactin / Q000097:blood / Q000378:metabolism*; D014176:Protein Biosynthesis; D051381:Rats; D011956:Receptors, Cell Surface / Q000187:drug effects; D012756:Sheep
D011956:Receptors, Cell Surface; D004958:Estradiol; D000324:Adrenocorticotropic Hormone; D011388:Prolactin; D013006:Growth Hormone; D003348:Cortisone