title: Endocrine-mediated parallel changes in hepatic glucocorticoid and prolactin receptors.
abstract: The objective of this study was to determine whether in female rat liver any relationship existed between prolactin and glucocorticoid receptors after hormonal manipulation. Bromocryptine (CB-154) treatment of adult SD female rats (80-100 days old) for 48 h decreased prolactin binding to hepatic membranes 49% and dexamethasone binding in hepatic cytosol 40% below control values. Administration of rat prolactin along with bromocriptine prevented these changes. In another study, prolactin binding to hepatic membranes increased 53% and dexamethasone binding in hepatic cytosol increased 113% above sham-control values, 3 days after adrenalectomy. On the other hand, hydrocortisone treatment of sham-operated rats reduced prolactin binding by 57% and dexamethasone binding by 76%. Scatchard analyses of the prolactin or dexamethasone binding data indicated that these manipulations changed the number of prolactin or dexamethasone binding sites rather than their apparent affinity constants. In vitro treatment of rat whole liver homogenate with various doses (10(-9) - 10(-5) M) of dexamethasone and corticosterone for 15 min at 22 degrees C resulted in a dose-dependent decrease in prolactin binding activity. However, direct addition of dexamethasone to a hepatic 15 000 X g to 100 000 X g membrane preparation exhibited no significant effects on prolactin binding. In conclusion, these studies show that (a) there is a parallel in vivo modulation of rat liver prolactin and glucocorticoid receptors under various experimental conditions and (b) in vitro exposure of whole liver homogenate to glucocorticoids inhibits the prolactin binding activity.
authors.forename: J R
authors.initials: JR
authors.lastname: Dave
authors.forename: R J
authors.initials: RJ
authors.lastname: Witorsch
authors.forename: M Y
authors.initials: MY
authors.lastname: Kalimi
mesh_terms: D000315:Adrenalectomy; D000818:Animals; D001971:Bromocriptine / Q000494:pharmacology*; D003345:Corticosterone; D003907:Dexamethasone / Q000378:metabolism / Q000494:pharmacology; D005260:Female; D005938:Glucocorticoids / Q000502:physiology*; D006854:Hydrocortisone / Q000494:pharmacology; D008099:Liver / Q000378:metabolism*; D011388:Prolactin / Q000378:metabolism / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D011956:Receptors, Cell Surface / Q000187:drug effects / Q000378:metabolism*; D011965:Receptors, Glucocorticoid / Q000187:drug effects / Q000378:metabolism*; D011981:Receptors, Prolactin; D011987:Receptors, Steroid / Q000378:metabolism*
chemical_list: D005938:Glucocorticoids; D011956:Receptors, Cell Surface; D011965:Receptors, Glucocorticoid; D011981:Receptors, Prolactin; D011987:Receptors, Steroid; D001971:Bromocriptine; D003907:Dexamethasone; D011388:Prolactin; D003345:Corticosterone; D006854:Hydrocortisone