Relationship between ACTH secretion and corticoid binding to specific receptors in perifused adenohypophyses.
This study reports on the kinetics of glucocorticoid-induced inhibition of ACTH release, together with steroid binding to specific pituitary receptors. It was shown that corticosterone (CORT) inhibited ACTH output provoked by either corticotropin-releasing factor (CRF) extracts or dbcAMP, in a manner which was both dose- and time-dependent. A close correlation appeared to exist between the degree of ACTH blockade and the percentage of filled steroid-binding sites. However, exposure of hypophyses to CORT for a critical period of time was a prerequisite for such a relationship to develop. Furthermore, it was found that dexamethasone (DEX) was more potent than CORT in inhibiting ACTH secretion and, in addition, bound to a greater extent to nuclei of pituitary cells. These data suggest the existence of a close correlation between occupancy of pituitary glucocorticoid receptors and modulation of ACTH secretion.
D000324:Adrenocorticotropic Hormone / Q000378:metabolism*; D000818:Animals; D003994:Bucladesine / Q000494:pharmacology; D002467:Cell Nucleus / Q000378:metabolism; D003345:Corticosterone / Q000494:pharmacology; D003346:Corticotropin-Releasing Hormone / Q000494:pharmacology; D003600:Cytosol / Q000378:metabolism; D003907:Dexamethasone / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D005938:Glucocorticoids / Q000494:pharmacology*; D007033:Hypothalamus, Middle / Q000378:metabolism; D008297:Male; D010903:Pituitary Gland, Anterior / Q000378:metabolism*; D051381:Rats; D011965:Receptors, Glucocorticoid / Q000378:metabolism*; D011987:Receptors, Steroid / Q000378:metabolism*; D014020:Tissue Extracts / Q000494:pharmacology
D005938:Glucocorticoids; D011965:Receptors, Glucocorticoid; D011987:Receptors, Steroid; D014020:Tissue Extracts; D003994:Bucladesine; D003907:Dexamethasone; D000324:Adrenocorticotropic Hormone; D003346:Corticotropin-Releasing Hormone; D003345:Corticosterone