Attenuated Pituitary -Endorphin Release in Estrogen-Treated Rats

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