PROGESTERONE, BUT NOT LHRH OR PROSTAGLANDIN-E(2), INDUCES SEQUENTIAL INHIBITION OF LORDOSIS TO VARIOUS LORDOGENIC AGENTS

In experiment I we studied the capacity of progesterone (P) and two no nsteroidal agents that activate lordosis, but do not bind to the proge stin receptor (PR), i.e. luteinizing hormone-releasing hormone (LHRH) and prostaglandin E2 (PGE2) to induce sequential inhibition (SI) in ov ariectomized estradiol-primed rats. The administration of 1 mg P, 5 mu g LHRH or 100 mug PGE2 induced significant lordosis within 4 h. An inj ection of 1 mg P, 24 h after the administration of the above lordogeni c agents, induced significant lordosis in rats pretreated with LHRH or PGE2, but not in those pretreated with P. Thus, only P induced SI (p < 0.025). In experiment II we investigated if progestin-induced SI res ults in a reduced capacity of the subjects to respond only to P or to other lordogenic agents. The synthetic progestin norgestrel (400 mug a dministered 24 h earlier) significantly reduced the responsiveness to P (p < 0.01), LHRH (p < 0.01), PGE2 (P < 0.025) and dibutyryl cyclic A MP (db cAMP p < 0.01). Results suggest that SI is triggered only by ag ents that bind to the PR (experiment I) and that it decreases the resp onsiveness of rats not only to P but also to other lordogenic agents ( experiment II).