scholarly journals Initiation of high dose gonadotrophin-releasing hormone antagonist treatment during the late follicular phase in the macaque abolishes luteal function irrespective of effects upon the luteinizing hormone surge

1997 ◽  
Vol 12 (3) ◽  
pp. 430-435 ◽  
Author(s):  
H. M. Fraser ◽  
S. F. Lunn ◽  
K. D. Morris ◽  
R. Deghenghi
1976 ◽  
Vol 83 (4) ◽  
pp. 684-691 ◽  
Author(s):  
Sven Johan Nillius ◽  
Leif Wide

ABSTRACT Modulating effects of oestradiol-17β and progesterone on the pituitary responsiveness to luteinizing hormone-releasing hormone (LRH) were investigated in 12 women with functional amenorrhoea. The pituitary reserve capacity for gonadotrophin section was investigated with repeated intravenous LRH tests before and after administration of oestradiol-1β followed by either progesterone or saline. Intramuscular injection of 1 mg of oestradiol-17β benzoate resulted in a suppression of both the basal gonadotrophin levels in serum and the gonadotrophin responses to LRH 24 h later. Progesterone, 25 mg im, was then administered in eleven experiments. Six h later, when the mean serum progesterone level had increased to levels similar to those seen in the early post-ovulatory phase of the menstrual cycle, there was a marked augmentation of the pituitary capacity to release both luteinizing hormone (LH) and follicle-stimulating hormone (FSH) in response to LRH. This was not found in eight experiments where saline was given instead of progesterone after oestrogen pretreatment. These findings suggest that the greatly increased pituitary sensitivity to LRH at midcycle may be caused not only by the oestradiol increase in blood during the late follicular phase but also in part by the small pre-ovulatory rise of progesterone during the mid-cyclic LH peak. Furthermore, they add further support to the hypothesis that progesterone as well as oestradiol is involved in the induction of the LH peak at midcycle. Progesterone may be of importance to secure the release of enough LH for ovulation and normal corpus luteum formation to occur.


1986 ◽  
Vol 109 (2) ◽  
pp. 155-161 ◽  
Author(s):  
J. E. A. McIntosh ◽  
R. P. McIntosh

ABSTRACT Our aim was to determine whether release of LH and FSH can be controlled differentially by the characteristics of applied signals of stimulatory gonadotrophin-releasing hormone (GnRH) alone, free of the effects of steroid feedback or other influences from the whole animal. The outputs of both gonadotrophins were significantly correlated (r≈0·90; P<0·0005) when samples of freshly dispersed sheep pituitary cells were perifused in columns for 7 h with medium containing a range of concentrations of GnRH in various patterns of pulses. Hormone released in response to the second, third and fourth pulses from every column was analysed in detail. Dose–response relationships for both LH and FSH were very similar when cells were stimulated with 5–8500 pmol GnRH/1 in 5-min pulses every hour. When GnRH was delivered in pulses at a maximally stimulating level, the outputs of both hormones increased similarly with increasing inter-pulse intervals. Efficiency of stimulation (release of gonadotrophin/unit stimulatory GnRH) decreased (was desensitized) with increasing pulse duration in the same way for both hormones. Thus, varying the dose, interval and duration of GnRH pulses did not alter the proportions of LH and FSH released in the short-term from freshly dissociated cells. However, the same cell preparations released more LH relative to FSH when treated with maximally stimulating levels of GnRH for 3 h in the presence of 10% serum from a sheep in the follicular phase of its ovulatory cycle compared with charcoal-treated serum. Because there was no gonadotrophin synthesis under the conditions used in vitro these results suggest that changes in the LH/FSH ratio seen in whole animals are more likely to result from differential clearance from the circulation, ovarian feedback at the pituitary, differential synthesis in intact tissue or another hormone influencing FSH secretion, rather than from differences in the mechanism of acute release controlled by GnRH. J. Endocr. (1986) 109, 155–161


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