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ABSTRACT
Ewes chronically treated with gonadotrophin-releasing hormone (GnRH) agonist were used to investigate the importance of the peripheral concentration of LH in FSH-stimulated follicular development. Twenty-four Welsh Mountain ewes were treated with two agonist implants containing 3·3 mg buserelin. During week 6 of treatment all the ewes were given a 72-h continuous infusion of ovine FSH alone (3 μg/h) or FSH with large (7·5 μg)- or small (2·5 μg) amplitude pulses of ovine LH delivered at 4-hourly intervals. The importance of baseline LH throughout the FSH infusion was evaluated in six animals which were treated with a specific antiserum against bovine LH (LH-AS) 15–20 h before the start of FSH treatment.
In the absence of LH-AS, infusion of FSH alone or with large or small pulses of LH stimulated the development of a normal number of small follicles (≤ 2·5 mm in diameter) and large follicles (> 2·5 mm in diameter). These follicles had normal diameter and steroid secretion compared with control ewes on day 8 of the luteal phase. In contrast, the animals pretreated with LH-AS developed no follicles > 2·0 mm in diameter but the number of small follicles per ewe was significantly (P < 0·05) increased.
These results support the hypothesis that FSH in the absence of pulsatile LH release stimulates preovulatory follicular development in ewes treated with GnRH agonist. The follicular response to LH pulses of different amplitude is dependent on both the stage of development of the follicle and the peripheral concentration of FSH. The endogenous basal level of LH present throughout the FSH infusion is essential for FSH to induce follicle growth beyond > 2·5 mm in diameter.
Journal of Endocrinology (1991) 128, 449–456
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ABSTRACT
The hypogonadotrophism model induced by the chronic administration of gonadotrophin-releasing hormone (GnRH) agonist was used to investigate the effects of different concentrations of FSH with or without LH pulses on the stimulation of follicular development in the ewe. Continuous administration of an agonist (buserelin) by osmotic minipump to thirty-six Welsh Mountain ewes from the early luteal phase for 5 weeks resulted in a sustained suppression of the plasma concentration of FSH and inhibited the pulsatile release of LH. The inhibition of gonadotrophin secretion was due to the desensitization and/or down-regulation of pituitary gonadotroph function, since the agonist-treated animals showed no response to a challenge of 1 μg GnRH.
During week 6 of agonist treatment, ewes were infused with either 4-hourly pulses of ovine LH (9 μg/pulse), low concentrations of ovine FSH (3 μg/h) or high concentrations of FSH (9 μg/h) alone or with 4-hourly pulses of LH. After 5 days of gonadotrophin infusion, there was no difference between the mean number of follicles per ewe from the animals treated with LH alone, low concentrations of FSH with or without LH pulses or the high concentration of FSH alone compared with the mean number of follicles from control ewes on day 8 of the luteal phase. Infusion of the high concentration of FSH alone stimulated the development of an increased number of large oestrogenic follicles (follicles > 2·5 mm in diameter and secreting > 3·7 nmol oestradiol/h in vitro) compared with control ewes. The addition of high-amplitude LH pulses to the infusion of the high concentration of FSH prevented follicles developing beyond 2·5 mm in diameter, but doubled the number of small follicles (≤2·5 mm) present in the ovaries.
These results show that normal follicular development can be induced by physiological concentrations of FSH alone in the absence of pulsatile LH release. The addition of high-amplitude LH pulses antagonized this stimulatory effect of FSH on follicle growth in the ewe.
Journal of Endocrinology (1990) 127, 273–283
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ABSTRACT
The study investigated the relationship between the plasma concentration of FSH and the stimulation of preovulatory follicle growth in vivo in ewes chronically treated with the gonadotrophin-releasing hormone (GnRH) agonist buserelin (HOE 766). Welsh Mountain ewes with regular oestrous cycles were treated for 6 weeks with two discs implants placed s.c., each containing 5 mg of the agonist in a matrix of polyhydroxybutyric acid. Treatment with the agonist for 35 days produced a sustained suppression of the plasma concentration of FSH, stopped the pulsatile release of LH and prevented follicular development beyond 2·5 mm diameter. There was no difference between the total number of follicles > 1·0 mm diameter present in the ovaries of GnRH agonist-treated ewes and day 8 luteal phase control ewes.
During the sixth week of agonist treatment ewes were infused with ovine FSH (6 μg NIADDK-oFSH16/h) in the presence of only basal concentrations of LH. After 24, 48, 72 or 120 h of FSH infusion, the mean number of follicles > 1 ·0 mm diameter per ewe was not significantly different between treated and control animals. Infusion of FSH caused a timedependent increase in (1) the number of follicles per ovary >2·5 mm, (2) the mean diameter of these follicles and (3) the proportion of the large follicles which could be classified as oestrogenic (> 3·7 nmol oestradiol/follicle per h in vitro). Injection of human chorionic gonadotrophin (750IU i.m.) after 120 h of FSH infusion caused the majority of these large follicles to ovulate and form apparently normal corpora lutea. These results indicate that, in the absence of pulsatile LH, FSH stimulates the growth of normal large oestrogenic follicles which, when stimulated, ovulate to produce viable corpora lutea.
Journal of Endocrinology (1990) 126, 297–307
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ABSTRACT
By selective removal and replacement of LH stimulation we sought to examine the relative importance of inhibin and oestradiol in controlling FSH secretion, and the role of LH in the control of ovarian hormone secretion, during the follicular phase of the oestrous cycle. Eight Finn–Merino ewes which had one ovary removed and the other autotransplanted to a site in the neck were given two injections of a gonadotrophin-releasing hormone (GnRH) antagonist (50 μg/kg s.c.) in the follicular phase of the cycle 27 h and 51 h after luteal regression had been induced by cloprostenol (100 μg i.m.). Four of the ewes received, in addition, i.v. injections of 2·5 μg LH at hourly intervals for 23 h from 42 to 65 h after GnRH antagonist treatment. Ovarian jugular venous blood samples were taken at 10-min intervals for 3 h before and 5 h after the injection of antagonist (24–32 h after cloprostenol) and from 49 to 53 h after antagonist (74–78 h after cloprostenol). Additional blood samples were taken at 4-h intervals between the periods of intensive blood sampling.
The GnRH antagonist completely inhibited endogenous pulsatile LH secretion within 1 h of injection. This resulted in a marked decrease in the ovarian secretion of oestradiol and androstenedione (P<0·001), an effect that was reversible by injection of exogenous pulses of LH (P<0·001). The pattern of ovarian inhibin secretion was episodic, but removal or replacement of stimulation by LH had no effect on the pattern or level of inhibin secretion. Peripheral concentrations of FSH rose (P<0·01) within 20 h of administration of the antagonist and these increased levels were maintained in ewes given no exogenous LH. In ewes given LH, however, FSH levels declined within 4 h of the first LH injection and by the end of the experimental period the levels of FSH were similar to those before administration of antagonist (P<0·01).
These results confirm that ovarian oestradiol and androstenedione secretion, but not inhibin secretion, is under the acute control of LH. We conclude that oestradiol, and not inhibin, is the major component of the inhibitory feedback loop controlling the pattern of FSH secretion during the follicular phase of the oestrous cycle in ewes.
Journal of Endocrinology (1990) 126, 377–384
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Abstract
The present study was designed to investigate the hormone profiles (oestradiol, LH, FSH, inhibin, progesterone) in high ovulating Meishan sows (MS; n = 9) and in contemporary Large-White hybrid control sows (LW; n = 9) during the follicular phase, the periovulatory period and the early luteal phase. Ovulation rate was higher in MS than LW animals (23·7 and 16·6 respectively; P<0·001) and overall was correlated with the area of the oestradiol peak (P<0·05) and inhibin concentrations (P<0·05). Both the duration of and the area of the oestradiol peak were greater in MS than LW (P<0·01; P<0·02), as were inhibin concentrations both before and after the LH surge (P<0·05). Neither basal nor peak concentrations of LH or FSH differed between the breeds (P>0·05), although FSH concentrations were correlated with the area under the oestradiol peak (P<0·05). Finally, the time-interval from the onset of the LH surge until the rise in plasma progesterone was shorter in MS than LW (54·5 and 74·3 h respectively; P<0·01). In conclusion, these results show for the first time that the higher ovulation rate in MS is associated with enhanced oestradiol and inhibin secretion with no significant difference in LH or FSH concentrations. The more rapid luteinization response to the LH surge by MS in terms of plasma progesterone concentrations may be important in ensuring the high level of embryo survival in this breed.
Journal of Endocrinology (1996) 150, 141–147