Metoclopramide-induced hyperprolactinaemia: effects on corpus luteum function, endometrial steroid receptor concentrations and 17 beta-hydroxysteroid dehydrogenase activity.

Abstract

Induced hyperprolactinaemia impairs ovarian follicular development, especially during the recruitment period. The consequences of hyperprolactinaemia during the luteal phase alone on corpus luteum function have not been characterized, nor have the actions of excessive circulating PRL on the endometrium. In this study, postovulatory 5-d administration of metoclopramide (MC) increased serum concentrations of PRL and decreased those of pregnenolone and progesterone indicating inhibition of steroidogenesis in the corpus luteum. This effect may partly explain the relatively common failure of implantation in association with induced ovulation using regimens leading to transient hyperprolactinaemia. In contrast to this, MC-induced hyperprolactinaemia during the mid-follicular (4 d) or early luteal phase of the cycle did not alter the concentrations of cytosol or nuclear oestrogen and progestin receptors or the activity of 17 beta-hydroxysteroid dehydrogenase in endometrial tissue. Thus, transiently elevated circulating PRL does not seem to have direct effects on female sex steroid receptors or their function in the proliferative or secretory endometrium.