Role of progesterone and nonsteroidal ovarian factors in regulating gonadotropin-releasing hormone self-priming in vitro

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Abstract

We investigated the effects of gonadotropin surge-attenuating factor (GnSAF), inhibin, and follistatin on GnRH self-priming and its augmentation by progesterone. Two GnRH challenges, 60 min apart, were administered to rat pituitary monolayers after 90-min exposure to medium alone (control), progesterone, GnSAF, inhibin, or follistatin. Inhibin-stripped follicular fluid from superovulated women was used as a source of GnSAF bioactivity. Under control conditions, the greater response to the second GnRH challenge (peak 2, 9.2 +/- 2.1; peak 1, 4.4 +/- 0.9 ng LH/mL; P < 0.01) demonstrated GnRH self-priming. None of the treatments significantly altered the first LH peak. Progesterone markedly increased GnRH self-priming (peak 2, 12.6 +/- 2.5 ng LH/mL; P < 0.01). However, GnSAF and RU486 significantly reduced GnRH self-priming (peak 2, 4.6 +/- 0.9 and 5.6 +/- 1.6 ng LH/mL, respectively; P < 0.01). The augmentation of self-priming induced by progesterone was completely abolished by coincubation with either GnSAF or RU486 (peak 2, 7.5 +/- 1.6 and 4.3 +/- 0.9 ng LH/mL, respectively; P < 0.01). Neither inhibin nor follistatin had any effect on GnRH self-priming or its augmentation by progesterone. The actions of RU486 in the presence and absence of progesterone demonstrate a nonprogestagenic effect of RU486 on the gonadotropes. In conclusion, the suppression of GnRH self-priming, with or without progesterone augmentation, supports the hypothesis that GnSAF acts by maintaining the pituitary in an unprimed state of reduced responsiveness to GnRH.

Original languageEnglish
Pages (from-to)1454-1459
Number of pages6
JournalJournal of Clinical Endocrinology and Metabolism
Volume81
Issue number4
Publication statusPublished - Apr 1996

Keywords

  • surge-attenuating factor
  • human follicular-fluid
  • secretion
  • women
  • LHRH
  • induction
  • midcycle
  • steroids
  • rats

Cite this

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title = "Role of progesterone and nonsteroidal ovarian factors in regulating gonadotropin-releasing hormone self-priming in vitro",
abstract = "We investigated the effects of gonadotropin surge-attenuating factor (GnSAF), inhibin, and follistatin on GnRH self-priming and its augmentation by progesterone. Two GnRH challenges, 60 min apart, were administered to rat pituitary monolayers after 90-min exposure to medium alone (control), progesterone, GnSAF, inhibin, or follistatin. Inhibin-stripped follicular fluid from superovulated women was used as a source of GnSAF bioactivity. Under control conditions, the greater response to the second GnRH challenge (peak 2, 9.2 +/- 2.1; peak 1, 4.4 +/- 0.9 ng LH/mL; P < 0.01) demonstrated GnRH self-priming. None of the treatments significantly altered the first LH peak. Progesterone markedly increased GnRH self-priming (peak 2, 12.6 +/- 2.5 ng LH/mL; P < 0.01). However, GnSAF and RU486 significantly reduced GnRH self-priming (peak 2, 4.6 +/- 0.9 and 5.6 +/- 1.6 ng LH/mL, respectively; P < 0.01). The augmentation of self-priming induced by progesterone was completely abolished by coincubation with either GnSAF or RU486 (peak 2, 7.5 +/- 1.6 and 4.3 +/- 0.9 ng LH/mL, respectively; P < 0.01). Neither inhibin nor follistatin had any effect on GnRH self-priming or its augmentation by progesterone. The actions of RU486 in the presence and absence of progesterone demonstrate a nonprogestagenic effect of RU486 on the gonadotropes. In conclusion, the suppression of GnRH self-priming, with or without progesterone augmentation, supports the hypothesis that GnSAF acts by maintaining the pituitary in an unprimed state of reduced responsiveness to GnRH.",
keywords = "surge-attenuating factor, human follicular-fluid, secretion, women, LHRH, induction, midcycle, steroids, rats",
author = "B Byrne and Fowler, {Paul Alfred Francois} and Allan Templeton",
year = "1996",
month = "4",
language = "English",
volume = "81",
pages = "1454--1459",
journal = "Journal of Clinical Endocrinology and Metabolism",
issn = "0021-972X",
publisher = "The Endocrine Society",
number = "4",

}

TY - JOUR

T1 - Role of progesterone and nonsteroidal ovarian factors in regulating gonadotropin-releasing hormone self-priming in vitro

AU - Byrne, B

AU - Fowler, Paul Alfred Francois

AU - Templeton, Allan

PY - 1996/4

Y1 - 1996/4

N2 - We investigated the effects of gonadotropin surge-attenuating factor (GnSAF), inhibin, and follistatin on GnRH self-priming and its augmentation by progesterone. Two GnRH challenges, 60 min apart, were administered to rat pituitary monolayers after 90-min exposure to medium alone (control), progesterone, GnSAF, inhibin, or follistatin. Inhibin-stripped follicular fluid from superovulated women was used as a source of GnSAF bioactivity. Under control conditions, the greater response to the second GnRH challenge (peak 2, 9.2 +/- 2.1; peak 1, 4.4 +/- 0.9 ng LH/mL; P < 0.01) demonstrated GnRH self-priming. None of the treatments significantly altered the first LH peak. Progesterone markedly increased GnRH self-priming (peak 2, 12.6 +/- 2.5 ng LH/mL; P < 0.01). However, GnSAF and RU486 significantly reduced GnRH self-priming (peak 2, 4.6 +/- 0.9 and 5.6 +/- 1.6 ng LH/mL, respectively; P < 0.01). The augmentation of self-priming induced by progesterone was completely abolished by coincubation with either GnSAF or RU486 (peak 2, 7.5 +/- 1.6 and 4.3 +/- 0.9 ng LH/mL, respectively; P < 0.01). Neither inhibin nor follistatin had any effect on GnRH self-priming or its augmentation by progesterone. The actions of RU486 in the presence and absence of progesterone demonstrate a nonprogestagenic effect of RU486 on the gonadotropes. In conclusion, the suppression of GnRH self-priming, with or without progesterone augmentation, supports the hypothesis that GnSAF acts by maintaining the pituitary in an unprimed state of reduced responsiveness to GnRH.

AB - We investigated the effects of gonadotropin surge-attenuating factor (GnSAF), inhibin, and follistatin on GnRH self-priming and its augmentation by progesterone. Two GnRH challenges, 60 min apart, were administered to rat pituitary monolayers after 90-min exposure to medium alone (control), progesterone, GnSAF, inhibin, or follistatin. Inhibin-stripped follicular fluid from superovulated women was used as a source of GnSAF bioactivity. Under control conditions, the greater response to the second GnRH challenge (peak 2, 9.2 +/- 2.1; peak 1, 4.4 +/- 0.9 ng LH/mL; P < 0.01) demonstrated GnRH self-priming. None of the treatments significantly altered the first LH peak. Progesterone markedly increased GnRH self-priming (peak 2, 12.6 +/- 2.5 ng LH/mL; P < 0.01). However, GnSAF and RU486 significantly reduced GnRH self-priming (peak 2, 4.6 +/- 0.9 and 5.6 +/- 1.6 ng LH/mL, respectively; P < 0.01). The augmentation of self-priming induced by progesterone was completely abolished by coincubation with either GnSAF or RU486 (peak 2, 7.5 +/- 1.6 and 4.3 +/- 0.9 ng LH/mL, respectively; P < 0.01). Neither inhibin nor follistatin had any effect on GnRH self-priming or its augmentation by progesterone. The actions of RU486 in the presence and absence of progesterone demonstrate a nonprogestagenic effect of RU486 on the gonadotropes. In conclusion, the suppression of GnRH self-priming, with or without progesterone augmentation, supports the hypothesis that GnSAF acts by maintaining the pituitary in an unprimed state of reduced responsiveness to GnRH.

KW - surge-attenuating factor

KW - human follicular-fluid

KW - secretion

KW - women

KW - LHRH

KW - induction

KW - midcycle

KW - steroids

KW - rats

M3 - Article

VL - 81

SP - 1454

EP - 1459

JO - Journal of Clinical Endocrinology and Metabolism

JF - Journal of Clinical Endocrinology and Metabolism

SN - 0021-972X

IS - 4

ER -