Glucocorticoid receptors and inhibition of serum prolactin by dexamethasone are reduced in rats with estrogen-induced pituitary tumors

In estrogen-induced pituitary tumors, binding of (3H)-dexamethasone (DEX) to soluble glucocorticoid receptors (GCR) was reduced 5-6 fold with respect to normal pituitaries. GCR in the tumors, however, bound normally to DNA-cellulose after heat-induced transformation. In control rats, serum prolactin...

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Detalles Bibliográficos
Autores principales: Piroli, G., Grillo, C., Lux de Lantos, V., Libertun, C., De Nicola, A.F.
Formato: JOUR
Materias:
dexamethasone
glucocorticoid receptor
prolactin
animal experiment
animal model
article
controlled study
feedback system
hypophysis tumor
male
nonhuman
priority journal
rat
Acceso en línea:http://hdl.handle.net/20.500.12110/paper_0172780X_v13_n2_p75_Piroli
Aporte de:
Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA) de Universidad de Buenos Aires
Descripción
Sumario:In estrogen-induced pituitary tumors, binding of (3H)-dexamethasone (DEX) to soluble glucocorticoid receptors (GCR) was reduced 5-6 fold with respect to normal pituitaries. GCR in the tumors, however, bound normally to DNA-cellulose after heat-induced transformation. In control rats, serum prolactin (PRL) increased after ether stress and decreased following DEX treatment, whereas these maneuvres failed to change the hyperprolactinemia of rats with pituitary tumors. Thus, in rats with experimental prolactinomas, impaired negative feedback of serum PRL to DEX seems to correlate with a low content of functional GCR.

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