Experimental evidence has recently accumulated indicating that administration of some prostaglandins (PGs), particularly those of the E and F series can evoke release of gonadotropic hormones (LH and FSH) and prolactin (PRL) by the anterior pituitary gland. Rather than acting on the pituitary directly, PGs are thought to exert their effects on the hypothalamus. In the case of LH and FSH they stimulate the release of lutenizing hormone-releasing hormone (LHRH). In the case of PRL, PGEs may act by inhibiting the release of PIF (prolactin-inhibiting factor) and/or by enhancing the release of PRF (prolactin-releasing factor). Pharmacologic inhibition of PG synthesis depresses the PRL release induced by estrogen without reducing pituitary PRL release from TRH. Blockade of PG synthesis also decreases LH release in a variety of circumstances, but does not inhibit the pituitary response to LHRH, thus supporting the concept that PGs may play a physiological role in the neural control of the release of this hormone. At the hypothalamus, PGE2 appears to stimulate LHRH release by acting directly on LHRH-secreting elements located in the medial basal hypothalamic-median eminence region (MBH-ME) and the preoptic-anterior hypothalamic (POA-AHA) areas. Radioimmunoassayable PGE and bicassayable PGF content of the ME of the rat is much greater than that of the MBH. Similarly, in vitro release of PGEs by the ME is several times greater than that of the MBH. In vitro incubation of MEs with norepinephrine (NE) results in PGE ands TI-release by the tissue. Inhibition of PG synthesis with indomethacin prevents not only the elevation in PGE levels induced by NE but also the increase in LHRH release induced by both dopamine (DA) and NE suggesting that PGs are physiologically involved in the process of neurotransmitter induced release of LHRH. Moreover, release of PGEs from the ME is reduced by incubation of the tissue with α-adrenergic or dopaminergic receptor blockers and the in vitro response of the ME LHRH terminals to PGEs is enhanced by in vivo pretreatment with ovarian steroids. In conclusion, these recent observations coupled to the aforementioned findings provide strong evidence in support of a physiological role for PGs in the hypothalamic control of gonadotropin release.
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