Release of oxytocin but not corticotrophin-releasing factor-41 into rat hypophysial portal vessel blood can be made opiate dependent

ABSTRACT The effects of morphine dependence and abrupt opiate withdrawal on the release of oxytocin and corticotrophin-releasing factor-41 (CRF-41) into hypophysial portal vessel blood in rats anaesthetized with urethane were investigated. Adult female Sprague–Dawley rats were made dependent upon morphine by intracerebroventricular infusion of morphine for 5 days; abrupt opiate withdrawal was induced by injection of the opiate antagonist naloxone. The basal concentrations of oxytocin in portal or peripheral plasma from morphine-dependent rats did not differ significantly from those in control, vehicle-infused rats. In rats in which the pituitary gland was not removed after stalk section, the i.v. injection of naloxone hydrochloride (5 mg/kg) resulted in a large and sustained increase in the concentration of oxytocin in both portal and peripheral plasma in control and morphine-dependent rats. The i.v. injection of naloxone resulted in a threefold increase in the secretion of oxytocin into portal blood in acutely hypophysectomized rats infused with morphine, but did not alter oxytocin secretion in vehicle-infused hypophysectomized rats. The concentration of oxytocin in peripheral plasma in both vehicle- and morphine-infused hypophysectomized rats was at the limit of detection of the assay and was unchanged by the administration of naloxone. There were no significant differences in the secretion of CRF-41 into portal blood in vehicle- or morphine-infused hypophysectomized rats either before or after the administration of naloxone. These data show that, as for oxytocin release from the neurohypophysis into the systemic circulation, the mechanisms which regulate oxytocin release into the portal vessel blood can also be made morphine dependent. The lack of effect of morphine or naloxone on the release of CRF-41 or other stress neurohormones suggests that the effect of opiate dependence and withdrawal is selective for oxytocin and is not simply a non-specific response to 'stress'. Journal of Endocrinology (1990) 124, 141–150

Levels of LH-releasing hormone in hypophysial stalk plasma during an oestrogen-stimulated surge of LH in ovariectomized rats

ABSTRACT Treatment of ovariectomized rats with 50 μg oestradiol benzoate, followed by 20 μg oestradiol benzoate 3 days later, induced surges of LH and FSH on the day following the second injection with oestradiol benzoate. During this surge of gonadotrophins, which was not blocked by the anaesthetic required to collect hypophysial stalk blood, increased hypophysial stalk plasma levels of immunoreactive LHRH were noted. Furthermore, the levels of LHRH in hypophysial portal blood were found to fluctuate. Measurement of LHRH in a pool of portal plasma revealed similar results when determined by radioimmunoassay and by a sensitive in-vitro bioassay. To mimic the observed release of LHRH during the surge of gonadotrophins, LHRH was infused, either systemically or directly into a long portal vessel, into oestrogen-treated, ovariectomized rats which had their endogenous release of LHRH blocked by pentobarbitone. An infusion of LHRH into the jugular vein, resulting in peripheral levels of LHRH which were somewhat lower than those measured in hypophysial stalk plasma, caused a surge of FSH similar to that found in rats used for collection of hypophysial stalk blood. When compared with the values in the latter animals, however, the levels of LH became two to four times higher by this infusion of LHRH. When LHRH was infused directly into a long portal vessel to mimic the observed secretion rate of LHRH during the oestrogen-stimulated surge of gonadotrophins, then the surges of LH and FSH were lower than those observed in the rats used for collection of stalk blood. J. Endocr. (1987) 112, 351–359