Inverse effects of corticosterone and thyroxine on glucocorticoid binding sites in the anterior pituitary gland.
The aim of this study was to determine whether pituitary glucocorticoid binding sites are under hormonal control. It was shown that corticosterone and thyroxine exerted antagonistic effects on both the transcortin-like component and true receptor present in the hypophysis: thyroid hormones, in contrast to glucocorticoids which exhibited opposite influence, increased maximum binding without affecting significantly the apparent association constant. Thus, it seems that the concentration of glucocorticoid binding sites is regulated by the glucocorticoid ligands, as well as by a different hormone. Moreover, a striking parallelism was found between plasma transcortin and pituitary transcotin-like capacity, argueing in favour of a plasma origin for this pituitary binder.
D000315:Adrenalectomy; D000324:Adrenocorticotropic Hormone / Q000494:pharmacology; D000818:Animals; D001665:Binding Sites / Q000187:drug effects; D003345:Corticosterone / Q000378:metabolism / Q000494:pharmacology*; D003600:Cytosol / Q000378:metabolism; D003907:Dexamethasone / Q000378:metabolism; D008297:Male; D010903:Pituitary Gland, Anterior / Q000378:metabolism*; D051381:Rats; D011965:Receptors, Glucocorticoid / Q000187:drug effects*; D011987:Receptors, Steroid / Q000187:drug effects*; D013965:Thyroidectomy; D013974:Thyroxine / Q000494:pharmacology*; D014156:Transcortin / Q000097:blood / Q000378:metabolism
D011965:Receptors, Glucocorticoid; D011987:Receptors, Steroid; D003907:Dexamethasone; D000324:Adrenocorticotropic Hormone; D014156:Transcortin; D013974:Thyroxine; D003345:Corticosterone