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OVINE CORTICOTROPHIN RELEASING FACTOR STIMULATES ACTH RELEASE FROM HUMAN CORTICOTROPHINOMA CELLS IN CULTURE; INTERACTION WITH HYDROCORTISONE AND ARGININE VASOPRESSIN
Author(s) -
WHITE M. C.,
ADAMS E. F.,
LOIZOU MARY,
MASHITER K.,
FAHLBUSCH R.
Publication year - 1985
Publication title -
clinical endocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.055
H-Index - 147
eISSN - 1365-2265
pISSN - 0300-0664
DOI - 10.1111/j.1365-2265.1985.tb00227.x
Subject(s) - medicine , endocrinology , vasopressin , arginine , hydrocortisone , adrenocorticotropic hormone , biological activity , basal (medicine) , neuropeptide , chemistry , in vitro , hormone , receptor , amino acid , biochemistry , insulin
SUMMARY We have investigated the effects of ovine corticotrophin releasing factor (oCRF) and its interaction with hydrocortisone (HC), and arginine vasopressin (AVP) on ACTH release from human corticotrophinoma cells in culture. Tumour tissue was obtained from six patients (three with active Cushing's disease and three with Nelson's syndrome). Cultures were maintained for periods of up to six months. Ovine CRF (21 nmol) significantly ( P >0·01) stimulated ACTH release from all tumours. Dose response (21 pmol‐21 nmol) effects were observed for the three tumours investigated over 2 and 4 h. Cortisol (20 μmol) significantly ( P >0·01) inhibited basal ACTH release from one tumour (Nelson's syndrome) by 75% over 4 h, and completely prevented the stimulatory effects of oCRF. AVP directly stimulated ACTH release from two tumours (Nelson's syndrome), and also potentiated the stimulatory action of oCRF during 30 min incubations. These data show corticotrophinoma cells from subjects with Cushing's disease and Nelson's syndrome can be directly stimulated by hypothalamic oCRF and may be potentiated by AVP. Cortisol and oCRF have been shown in one tumour to have antagonistic actions at the pituitary level.