Gonadotropin-releasing hormone antagonist administration enhances gonadotrope responsiveness at doses inadequate to suppress immunoassayable gonadotropin levels.
Chronic GnRH antagonist therapy produces enhanced gonadotrope responsiveness to supraphysiologic stimuli despite the lack of any measurable suppression of gonadotropin levels. This indicates that GnRH antagonists fundamentally alter gonadotrope response mechanisms without inhibiting gonadotropin release. Beyond the physiologic implications, these data may eventually impact the development of clinical protocols. Benefits could include enhancements in the endogenous gonadotropin flare during controlled ovarian hyperstimulation cycles. Additionally, proposed contraceptive protocols where GnRH antagonists are used to produce the initial inhibition in gonadotropin release and are then followed by a GnRH-a (to avoid the gonadotropin flare) may in fact produce paradoxical results.
Scott
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Division of Physiology and Medicine, Southwest Foundation for Biomedical Research, San Antonio, Texas.
Illions
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EH
Carey
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KD
Navot
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D
D000818:Animals; D005260:Female; D005640:Follicle Stimulating Hormone / Q000097:blood*; D007987:Gonadotropin-Releasing Hormone / Q000037:antagonists & inhibitors*; D007700:Kinetics; D016729:Leuprolide / Q000494:pharmacology; D007986:Luteinizing Hormone / Q000097:blood*; D009842:Oligopeptides / Q000494:pharmacology; D010215:Papio
D009842:Oligopeptides; D007987:Gonadotropin-Releasing Hormone; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone; C057022:iturelix; D016729:Leuprolide