HYPOTHALAMIC RELEASE OF ATRIAL-NATRIURETIC-FACTOR AND BETA-ENDORPHIN INTO RAT HYPOPHYSEAL PORTAL PLASMA - RELATIONSHIP TO ESTROUS-CYCLE AND EFFECTS OF HYPOPHYSECTOMY

The release of beta-endorphin and atrial natriuretic factor (ANF) into hypophysial portal plasma was investigated in male and female Wistar rats. The principal aim of the study was to investigate the possible role of beta-endorphin and ANF in the hypothalamic control of LH and prolactin secretion. In male rats, anaesthetized with urethane, the concentrations of beta-endorphin in portal blood collected immediately after hypophysectomy were within the same range as those in peripheral plasma. Furthermore, electrical stimulation of the median eminence did not increase the portal plasma concentrations of beta-endorphin. In female rats, anaesthetized with alphaxalone, the portal plasma concentrations in long-term (6-8 weeks) or acutely hypophysectomized rats were significantly greater than those in peripheral plasma. In acutely hypophysectomized female rats the concentrations and contents of beta-endorphin in portal plasma collected at 10.00-11.30 h of pro-oestrus were significantly (approximately sixfold) greater than at dioestrus or at 20.00-21.00 h of pro-oestrus, but these changes were not consistently seen in all experiments. In female rats in which the pituitary gland was not removed for portal blood collection, portal plasma contents of ANF remained unchanged throughout the day of pro-oestrus, suggesting that it is unlikely that ANF is involved in the spontaneous LH or prolactin surge. The effects of ovarian steroids on the secretion of hypothalamic ANF and beta-endorphin were determined by measuring the portal plasma concentration of ANF and beta-endorphin on the morning of presumptive pro-oestrus in rats ovariectomized 24 h previously and injected with either oil or oestradial benzoate (OB). Portal plasma contents of ANF were significantly lower in OB- compared with oil-treated rats, suggesting that oestradiol inhibits ANF release into rat hypophysial portal plasma. In contrast, there were no significant between-group differences in the content or concentration of beta-endorphin in portal plasma. Thus, the increased beta-endorphin in the portal plasma of some of the intact animals during the morning of pro-oestrus is not due to the preovulatory surge of oestradiol-17-beta. The output of beta-endorphin into portal blood in long-term hypophysectomized rats was lower than in dioestrous or pro-oestrous rats in which the pituitary gland was removed immediately before portal blood collection. Taken together, these results suggest that beta-endorphin release into portal plasma may depend upon normal physiological levels of pituitary and pituitary-dependent hormones in the circulation, and that beta-endorphin release into portal blood is not controlled by short- or long-loop negative feedback. In sum, these data confirm that in adult female rats, ANF and beta-endorphin are released into hypophysial portal plasma and show (i) that the secretion of ANF, but not of beta-endorphin, can be affected by oestradiol, (ii) that the concentrations of ANF in portal plasma are sufficient to affect the release of pituitary hormones but are not related to plasma concentrations of LH and prolactin during the afternoon of pro-oestrus, (iii) that whilst there is no simple inverse relationship between beta-endorphin overflow into portal plasma and LHRH secretion, the increased release of beta-endorphin during the morning of pro-oestrus may be consistent with a role for this peptide in triggering the pro-oestrous surge of prolactin, and (iv) that a sex difference in beta-endorphin release into portal plasma is suggested by the absence of beta-endorphin in the portal plasma of male rats.