Release of prostaglandin E2 and beta-endorphin-like immunoreactivity from rat adenohypophysis in vitro: variations after adrenalectomy or lesions of the paraventricular nuclei.

Previous studies in vitro have shown that prostaglandin (PG) E2 is formed in rat adenohypophysis upon stimulation by arginine-vasopressin (AVP) and synthetic ovine corticotropin-releasing factor (CRF-(1-41]. The aim of the present study was to examine whether long-term changes in the hypothalamic stimulation of the pituitary corticotrophs in vivo may influence PG synthesis in subsequent in vitro incubations of rat anterior pituitary quarters. The release of PGE2 from adenohypophyses obtained from adrenalectomized rats was increased to about 300% of controls both under basal conditions and after stimulation by AVP; by contrast, the release of PG D2 was changed neither by adrenalectomy nor by AVP. Simultaneously, basal release of beta-endorphin-like immunoreactivity (beta-EI) was increased after adrenalectomy to about 300% of controls, parallel to the increase in the tissue content, whereas AVP-induced beta-EI release was unchanged. Addition of PG E2 inhibited, whereas blockade of PG formation by indomethacin enhanced AVP-induced beta-EI release both in controls and after adrenalectomy. When anterior pituitary glands were taken from rats with lesions of the paraventricular nuclei, release of PG E2 was decreased as compared to controls both under basal conditions and after stimulation by AVP or CRF-(1-41). Simultaneously, basal and evoked release of beta-EI was unchanged. We conclude that the formation of PG E2 in the adenohypophysis varies according to long-term changes in the hypothalamic stimulation of adrenocorticotropin and beta-endorphin release supporting the view that PG E2 synthesis is related to, and may be involved in mechanisms controlling peptide hormone release from the corticotrophs.