Antifolliculogenic action of progesterone despite hypersecretion of FSH in monkeys

1982 ◽  
Vol 243 (5) ◽  
pp. E387-E397 ◽  
Author(s):  
A. L. Goodman ◽  
G. D. Hodgen

To learn how progesterone (P) inhibits follicle growth during the luteal phase, we determined whether P will inhibit follicle growth when follicle-stimulating hormone (FSH) is secreted in large amounts, namely, after luteectomy (CLX) in monkeys with only one ovary. Second, a functional role for 17 alpha-hydroxyprogesterone (17OHP) was examined as a common mediator of the inhibition of folliculogenesis by the dominant follicle and corpus luteum. To accomplish the first goal, nine chronically hemiovarectomized monkeys were lutectomized chronically hemiovariectomized monkeys were luteectomized at midluteal phase. In five monkeys that received no steroid, the next preovulatory luteinizing hormone (LH) surge occurred 14.0 +/- 0.8 days (mean +/- SE) after CLX. In contrast, the next LH surge was delayed in four monkeys implanted for 10 days with Silastic capsules containing P and occurred 25.0 +/- 2.7 days after CLX, i.e., 14.8 +/- 2.7 days after the capsule removal. In both groups, FSH levels increased markedly after CLX to a comparable degree and duration; yet, only a single follicle ovulated in each monkey. To examine a potential inhibitory role for 17OHP, monkeys with two ovaries were luteectomized and received 1) no steroid, 2) 17OHP via Silastic capsules, or 3) P for 10 days after CLX. Progesterone replacement after CLX appeared to maintain 17OHP levels, which showed a transient decrease after CLX alone. As above, P delayed the next LH surge (25.4 +/- 1.3 vs. 15.0 +/- 0.6 days) despite comparable increases in serum FSH after CLX alone. Replacement at two levels of 17OHP did not delay the onset of menses (2-3 days post-CLX) or significantly delay the next LH surge 18.3 +/!- 1.9 or 20.8 +/- 3.4 vs. 15.0 +/- 0.6 days (P greater than 0.2) in monkeys CLX only. Whatever may be the mode of action of P, it appears that it is not mediated by peripheral conversion to 17OHP. These findings demonstrate that P at luteal phase levels can inhibit follicle growth culminating in ovulation even in the face of sustained, elevated levels of endogenous FSH. Because single ovulations occurred despite unambiguous and prolonged increments in serum FSH after CLX, the precise regulation of the ovulatory quota in this primate appears to be accomplished by means other than FSH alone.

2002 ◽  
Vol 82 (4) ◽  
pp. 599-602 ◽  
Author(s):  
R. Ungerfeld ◽  
A. Pinczak ◽  
M. Forsberg ◽  
E. Rubianes

Ovarian responses to the "ram effect" were characterized in 11 anestrous Corriedale ewes. In seven ewes, there was a luteinizing hormone (LH) surge 36.7 ± 12.3 h (mean ± SEM) after ram introduction and a concurrent increase (P < 0.05) in serum follicle stimulating hormone (FSH). Ovarian responses (monitored ultrasonographically) were highly variable. One ewe had two luteal phases (short and normal, respectively), three had delayed ovulation (days 5–7), two had luteinization of non-ovulatory follicles, one developed a luteinized follicular cyst, and four had no luteal phase. Key words: Ram effect, ovarian follicular dynamics, seasonal anestrus, ultrasonography, gonadotropin


1982 ◽  
Vol 243 (4) ◽  
pp. E325-E331 ◽  
Author(s):  
A. L. Goodman ◽  
M. J. Koering ◽  
W. E. Nixon ◽  
R. F. Williams ◽  
G. D. Hodgen

Previous work demonstrated that asymmetrical ovarian activity accompanies morphological asymmetry during the ovarian cycle in rhesus and cynomolgus macaques. This study was designed to determine whether functional ovarian asymmetry could be used to detect the upcoming dominant follicle (DF) even before it was grossly visible. Revealing a latent DF in this manner would permit a better estimate of the time when dominance of the follicle selected to ovulate is attained. To accomplish this, rhesus monkeys were luteectomized at midluteal phase to synchronize subsequent follicle growth, and 4 or 8 days later either the ipsilateral or contralateral ovary was removed. Unilateral ablation at day 4 (when no DF is grossly apparent) of either ovary produced symmetrical responses: the interval from luteectomy (CLX) to the next luteinizing hormone (LH) surge was extended by about 4 days in both groups (P less than 0.01), i.e., from about 12.5 days to 16.7 +/- 1.6 and 17.0 +/- 1.5 days (mean +/- SE). In contrast, hemiovariectomy at day 8 produced markedly divergent asymmetrical responses. Removal of the ipsilateral ovary 8 days after CLX did not affect the timing of the next LH surge (13.2 +/- 0.6 days), which ordinarily occurs about 12.5 days after CLX alone. However, ablation of the contralateral ovary (bearing the next DF) on day 8 extended the interval from CLX to the next LH surge from about 12.5 to 26.6 +/- 1.3 days. These findings indicate that, during the normal ovarian cycle when menses occurs 2--4 days after luteolysis, the follicle destined to ovulate becomes dominant between the 2nd and 6th day and that attainment of dominance signals the completion of a follicle selection process that begins or resumes promptly after luteolysis.


1989 ◽  
Vol 67 (2) ◽  
pp. 135-139 ◽  
Author(s):  
Richard F. Weick ◽  
Vaclav Pitelka ◽  
David L. Thompson

Experiments were performed to study the responsiveness of the pituitary to gonadotropin-releasing hormone (GnRH) during the dynamic changes in gonadotropin secretion associated with the estrogen-induced luteinizing hormone (LH) surge in the ovariectomized (OVX) rhesus monkey. Silastic capsules filled with estradiol-17-β were implanted subcutaneously in ovariectomized rhesus monkeys, resulting in an initial lowering of circulating LH and follicle-stimulating hormone (FSH) concentrations followed by an LH–FSH surge. GnRH was injected intravenously just before estrogen implantation, during the negative feedback response and during the rising, the peak, and the declining phases of the LH surge. The LH and FSH responses during the negative feedback phase were as large as those before estrogen treatment (control responses). During the rising phase of the LH surge, the acute response to GnRH injection did not differ significantly from the control response, but the responses 60 and 120 min after injection were somewhat increased. During the declining phase of the LH surge, the pituitary was not responsive to exogenous GnRH, although LH probably continued to be secreted at this time since the LH surge decreased more slowly than predicted by the normal rate of disappearance of LH in the monkey. We conclude that an increased duration of response to GnRH may be an important part of the mechanism by which estrogen induces the LH surge, but we do not see evidence of increased sensitivity of the pituitary to GnRH as an acute releasing factor at that time.Key words: LH surge, GnRH, FSH, ovariectomized monkey.


Zygote ◽  
2017 ◽  
Vol 25 (3) ◽  
pp. 235-243 ◽  
Author(s):  
Maxim Filatov ◽  
Yulia Khramova ◽  
Elena Parshina ◽  
Tatiana Bagaeva ◽  
Maria Semenova

SummaryGonadotropins are the key regulators of ovarian follicles development. They are applied in therapeutic practice in assisted reproductive technology clinics. In the present review we discuss the basic gonadotropic hormones – recombinant human follicle-stimulating hormone, its derivatives, luteinizing hormone and gonadotropin serum of pregnant mares, their origin, and application in ovarian follicle systems inin vitroculture systems.


2018 ◽  
Author(s):  
Rebecca Pierson ◽  
Kelly Pagidas

A normal menstrual cycle is the end result of a sequence of purposeful and coordinated events that occur from intact hypothalamic-pituitary-ovarian and uterine axes. The menstrual cycle is under hormonal control in the reproductively active female and is functionally divided into two phases: the proliferative or follicular phase and the secretory or luteal phase. This tight hormonal control is orchestrated by a series of negative and positive endocrine feedback loops that alter the frequency of the pulsatile secretion of gonadotropin-releasing hormone (GnRH), the pituitary response to GnRH, and the relative secretion of luteinizing hormone and follicle-stimulating hormone from the pituitary gonadotrope with subsequent direct effects on the ovary to produce a series of sex steroids and peptides that aid in the generation of a single mature oocyte and the preparation of a receptive endometrium for implantation to ensue. Any derailment along this programmed pathway can lead to an abnormal menstrual cycle with subsequent impact on the ability to conceive and maintain a pregnancy. This review contains 7 figures and 26 references Key words: follicle-stimulating hormone, follicular phase, gonadotropin-releasing hormone, luteal phase, luteinizing hormone, menstrual cycle, ovulation, progesterone, proliferative phase, secretory phase


1986 ◽  
Vol 43 (1) ◽  
pp. 101-107 ◽  
Author(s):  
S. M. Rhind ◽  
I. D. Leslie ◽  
R. G. Gunn ◽  
J. M. Doney

ABSTRACTTwo groups of 19 Border Leicester cf × Scottish Blackface 9 ewes were fed so that ewes of one group were in a very high level of body condition at mating (mean score 3·35) and had a high level of intake. Ewes of the second group were in moderately high condition (mean score 2·74) and were given a live-weight maintenance ration. Ewes in the high group had a higher ovulation rate than those of the moderate group (3·36 v. 2·33) but a lower number of embryos per ewe mated (1·16 v. 1·42). Mean follicle stimulating hormone profiles were similar for ewes of the two groups during the luteal and follicular phases of the cycle before mating and during the subsequent oestrus. Mean prolactin concentrations were higher in ewes of the high group during the follicular phase and oestrus but not during the luteal phase. Mean luteinizing hormone (LH) concentrations were higher in ewes of the high group during the follicular phase and oestrus but not during the luteal phase. Mean LH concentrations were similar for the two groups at all times but the frequency of LH pulses was higher in the high group during the follicular phase.Ewes that were not pregnant at slaughter had abnormal progesterone profiles following mating, abnormal pre-ovulatory LH surges or failed to show oestrus. These abnormalities were not related to gonadotrophin profiles prior to oestrus.


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