Effect of sex steroids on beta-endorphin in hypophyseal portal blood.

Abstract

Previous studies in female monkeys have shown that beta-endorphin (beta-EP) of hypothalamic origin is present in high concentrations in the hypophyseal portal blood and declines at the time of menses and after ovariectomy. In this study we have examined the effects of estradiol and progesterone replacement on portal blood beta-EP in ovariectomized monkeys. After acute iv administration of estradiol (2 micrograms), beta-EP did not rise from previously low levels (less than 133 pg/ml) over the ensuing 3 h. After chronic estradiol replacement for 3 weeks, portal beta-EP was detectable in 2 of 4 ovariectomized monkeys, with peak values of 341 and 733 pg/ml, respectively. When progesterone as well as estradiol were replaced chronically, high levels of beta-EP, [1610 +/- 192 (SE) pg/ml] were measured in all 13 portal blood samples collected from 4 ovariectomized monkeys. The majority of the beta-EP immunoactivity in these samples eluted from a Sephadex G-50 column in the same position as synthetic human beta-EP. Cation exchange chromatography showed that the majority of immunoactive beta-EP in portal plasma appeared to be nonacetylated beta-EP (1-31). We conclude that ovarian steroids are necessary for the release of hypothalamic beta-EP into portal blood and suggest that cyclic changes in sex steroids may affect anterior pituitary function in part via a mechanism involving hypothalamic beta-EP.