Attenuated Pituitary β-Endorphin Release in Estrogen-Treated Rats

Abstract

Abstract

Using a newly developed radioimmunoassay for β-endorphin (β-END) the influence of gonadal steroids and sex difference on basal and stimulated β-END secretion was investigated. Administration of estradiol benzoate (EB), but not testosterone proprionate, tended to decrease resting levels of plasma β-END and significantly attenuated the stress-induced increase in circulating β-END in male rats. Consistent with these findings is the observation that female rats had somewhat lower nonstress and stress-elevated levels of plasma β-END as compared to males. Over 95% of the total pituitary content of β-END (12.7 ± 1.7 μg) was found to be present in the neurointermediate lobe (NIL) and treatment with EB for 5 days significantly decreased (by up to 56%) stores of β-END in the NIL yet had no effect on the small amount of β-END present in the pars distalis (PD). Since daily administration of EB produced dose-related increases in plasma levels of corticosterone and dexamethasone treatment completely prevented the stress-induced release of β-END, a possible mechanism by which treatment with EB results in decreased β-END secretion may be related to the ability of estrogen to increase circulating levels of adrenal glucocorticoids. Together, these findings suggest that adrenal glucocorticoids may be responsible for the diminished release of β-END observed here in female rats and those treated with EB as compared to normal male rats. In addition, the very high concentration of β-END in the NIL as compared to the PD provides indirect evidence for the pars intermedia being the primary source of circulating β-END in the rat.