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Prostaglandin F (PGF2α) has been shown to be luteolytic in sheep when infused into the ovarian artery in situ (Thorburn & Nicol, 1971) or when autotransplanted to the neck (McCracken, Glew & Scaramuzzi, 1970). It was originally suggested that PGF2α might induce luteal regression by causing venoconstriction in the utero-ovarian vein and hence an alteration in ovarian blood flow (Pharriss & Wyngarden, 1969). Variable changes in total ovarian blood flow have been described after intra-arterial infusion of PGF2α in sheep (McCracken et al. 1970; Chamley, Buckmaster, Cain, Cerini, Cerini, Cumming & Goding, 1972).

Prostaglandin F was infused into the ovary through the ovarian artery at a dose of 40 μg/h in nine experiments in four ewes with autotransplanted ovaries. Ovarian blood flow and progesterone secretion rate were measured, as previously described (Collett, Land & Baird, 1973), at intervals during and immediately after a 4 h infusion (Fig. 1).

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A. S. McNeilly and D. T. Baird


Changes in the plasma concentration of inhibin were measured by radioimmunoassay in ovarian venous blood collected at 10-min intervals for 5-h periods between 16 and 21 h and 40 and 45 h after cloprostenol-induced luteal regression in six Finn–Merino sheep. Episodes of inhibin secretion occurred with an interpulse interval of 66 ± 5 min in both stages of the follicular phase. These changes in inhibin were unrelated to pulses of LH or oestradiol. There was no relationship with plasma concentrations of FSH, which did not change in a pulsatile manner. These results suggest that the release of inhibin by the preovulatory follicle(s) occurs in a pulsatile manner and is under local control by unknown factors.

Journal of Endocrinology (1989) 122, 287–292

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The concentrations of FSH, oestradiol and androstenedione in the follicular fluid of normal and cystic human follicles were measured at different stages of the menstrual cycle. In addition, the number of granulosa cells in the follicles was determined.

In follicles in which FSH was detectable, the concentration of oestradiol was greater than that of androstenedione, irrespective of the stage of the cycle. In contrast, in those follicles in which FSH was undetectable and in all cystic follicles irrespective of the level of FSH, the concentration of androstenedione was greater than that of oestradiol. In follicles containing FSH there was a highly significant linear correlation between the number of granulosa cells and the concentration of follicular oestradiol (P < 0·001).

It is suggested that in human ovaries up to 90% of the oestradiol in follicular fluid may originate from the granulosa cells.

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The secretion rates of oestradiol, androstenedione and progesterone and the peripheral plasma concentration of LH were measured in 12 ewes with ovarian autotransplants before and after luteal regression induced by a single intramuscular injection of a synthetic prostaglandin (PG) analogue, 16-aryloxyprostaglandin F (I.C.I. 80996). Luteal regression was followed by a fourfold rise in the basal concentration of LH and increased secretion of oestradiol. In five out of six ewes there was a discharge of LH with the peak occurring 36–78 h after the injection of the PG analogue. The secretion of oestradiol declined from 3·68± 1·08 to 0·33± 0·6 (s.e.m.) ng/min in the 24 h following the LH peak (P < 0·001). In the remaining six ewes in which progesterone was implanted subcutaneously 24 h after the injection of PG analogue, follicular development was suppressed as indicated by the low secretion of oestradiol and androstenedione. The basal concentration of LH fell to values similar to those observed during the luteal phase after the implant of progesterone. The secretion of androstenedione followed a similar pattern to that of oestradiol in those ewes which showed presumptive evidence of ovulation. These results suggest that progesterone reinforces the negative feedback effects of oestrogen in the ewe.

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The response of the ovine corpus luteum to repeated infusions of luteinizing hormone (LH) or of human chorionic gonadotrophin (HCG) was tested in four ewes with the left ovary autotransplanted to the neck. Constant infusion for 1 h of either LH (100 or 1000 μg/h) or HCG (200 i.u./h) via the ovarian artery stimulated a temporary increase in secretion of progesterone which fell to control levels by 60 min. Ovarian blood flow increased progressively (P < 0·05) throughout the infusion of gonadotrophin in three of the five experiments. A second infusion of either gonadotrophin after a further control hour failed to stimulate progesterone secretion. These results suggest that ovine luteal tissue rapidly becomes refractory to the steroidogenic effect of LH in vivo.

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The PO2, PCO2, pH and oxygen content were measured in blood from the carotid artery, and jugular and ovarian veins of six sheep with cervical ovarian autotransplants. The PO2 in ovarian venous blood (56·0 ± 3·9 (s.e.m.) mmHg) was lower than that in carotid arterial blood (94·3 ± 8·3) but higher than that in jugular venous blood (43·4 ± 3·1). The oxygen content of ovarian venous blood was significantly higher than that of jugular venous blood. The high PO2 and oxygen content in ovarian venous relative to jugular venous blood together with the high blood flow suggests the possibility of arterio-venous shunts within the ovary or its vascular pedicle.

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T. A. Bramley, G. S. Menzies, and D. T. Baird


The effects of a number of analogues of gonadotrophin-releasing hormone (GnRH) on the binding of a radiolabelled GnRH agonist (GnRH-A; d-Ser(But)6, des Gly10]GnRH-ethylamide) to homogenates of human corpus luteum (CL) and rat pituitary tissue were compared. Specific binding was inhibited by GnRH and GnRH-like peptides only. Both the C-terminal amide and N-terminal region of the GnRH molecule were required for binding in both tissues. However, amino acid substitutions at position 6 markedly enhanced, and at position 8 markedly reduced, binding potencies in rat pituitary tissue compared with human CL binding sites. These results indicate that GnRH-binding sites of rat pituitary and human luteal tissue have a similar degree of specificity for GnRH-like peptides, and a similar requirement for both N- and C-terminal regions of the peptide, but that differences in specificity related to the mid-chain region of GnRH exist between human luteal and rat pituitary binding sites.

J. Endocr. (1985) 000, 000–000

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T. A. Bramley, D. Stirling, I. A. Swanston, G. S. Menzies, and D. T. Baird


The specific binding of 125I-labelled human chorionic gonadotrophin (hCG), human low-density lipoprotein (hLDL), human FSH (hFSH) and human prolactin (hPRL) to homogenates of human corpus luteum tissue was measured.

Specific binding of 125I-labelled hCG was dependent on the temperature and duration of incubation, was inhibited by divalent metal ions or chelating agents, and increased linearly with homogenate concentration. Recovery of bound hormone was more effective using Millipore filtration or polyethylene glycol precipitation compared with centrifugation alone. Binding of 125I-labelled hCG was inhibited specifically by low levels of hCG and human LH (hLH) but not by ovine LH or bovine LH. Incubation of human luteal tissue with ice-cold citrate buffer (pH 3) released more than 90% of specifically bound 125I-labelled hCG within 5 min. This treatment inactivated LH receptors, but did not affect the immunoactivity of hLH released, enabling the measurement of released hormone by radioimmunoassay.

Scatchard plots of binding of 125I-labelled LDL to human corpus luteum demonstrated a single class of binding sites. Binding was saturable, increased linearly with increasing concentration of homogenate, and was displaceable by low concentrations of unlabelled LDL.

Binding of 125I-labelled hPRL to human luteal homogenates was increased by Mg2+ and was specific for lactogenic hormones (human prolactin, human growth hormone and ovine prolactin). Binding of 125I-labelled hFSH was not dependent on divalent metal ion concentration (in marked contrast to hFSH binding to immature pig granulosa cell receptors) and was displaced by hFSH preparations but not by hPRL, ovine LH or hCG at 1 μg/ml.

These results establish optimal conditions and hormone specificities for the measurement of human luteal gonadotrophin and LDL receptors, and methods for the estimation of hLH/hCG endogenously bound to human corpus luteum tissue.

J. Endocr. (1987) 113, 305–315

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T A Bramley, D Stirling, G S Menzies, and D T Baird

Scottish Blackface ewes were synchronised in mid-breeding (November; group 1; n=12 ewes) or late-breeding season (March; group 2; n=16). Anoestrous ewes (May) were treated with progestagen sponges for 7 days and then given 250 ng GnRH 3-hourly for 24 h, 2-hourly for 24 h and hourly for a further 24 h (group 3; n=12). A second group of anoestrous ewes (group 4, n=19) received three bolus injections (30 μg) of GnRH at 90-min intervals without progestagen pretreatment. After ovulation, ewes were bled twice daily until slaughter (day 4 or day 12: oestrus=day 0). Mid-breeding season (group 1) and anoestrous ewes in group 3 formed ‘adequate’ corpora lutea (CL) with high plasma progesterone levels (3–4 ng/ml) maintained for at least 12 days, and responded in vivo to ovine LH (oLH) (10 μg) with a rise in plasma progesterone on day 11 (group 3, but not group 1, ewes also responded on day 3). CL minces from these ewes responded to human chorionic gonadotrophin (hCG) in vitro with a dose-dependent increase in progesterone secretion. Ewes in group 4 had a foreshortened luteal phase (8–10 days) and low plasma progesterone levels (~1 ng/ml), consistent with formation of inadequate CL. LH injection failed to induce a significant plasma progesterone increase. Furthermore, although progesterone secretion in vitro in response to maximally stimulating doses of hCG or dibutyryl cAMP (dbcAMP) was similar to that in adequate CL, the sensitivity of these CL to hCG (EC (effective concentration)50, 1 IU hCG/ml) was reduced 10-fold compared with adequate CL (EC50, 0.1 IU hCG/ml; P<0.01). Ewes that ovulated in the late breeding season (group 2) had high plasma progesterone, although levels began to decrease after day 10. Injection of oLH in vivo increased plasma progesterone. However, sensitivity to hCG in vitro (EC50, 0.5 IU hCG/ml) was intermediate between that of adequate luteal tissue (groups 1 and 3; EC50, 0.1 IU/ml) and that of group 4 ewes (EC50, 1 IU hCG/ml). Our data demonstrate a markedly reduced luteal sensitivity to LH in vivo and hCG in vitro in Scottish Blackface ewes with inadequate CL, and suggest that a similar loss of sensitivity to LH may occur in the late breeding season.

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G. E. Mann, A. S. McNeilly, and D. T. Baird


This experiment was undertaken in order to investigate the production of inhibin, oestradiol and androstenedione by ovarian follicles at different stages of the oestrous cycle in sheep. Twenty-four Scottish Blackface ewes were allocated to four groups of six ewes, i.e. those operated on during the luteal phase (day 10), and those operated on during the follicular phase 24–30, 36 and 60 h after the induction of luteal regression by an injection of 125 μg cloprostenol on day 10 of the luteal phase. Samples of jugular and ovarian venous blood were collected under anaesthesia and ovaries were then removed and all follicles larger than 3 mm diameter dissected out and incubated in medium for 2 h.

After injection of cloprostenol, luteal regression occurred as indicated by a fall in the secretion rate of progesterone. The ovarian secretion rate of inhibin was similar at all stages of the follicular phase and during the luteal phase while, in contrast, the secretion rate of oestradiol was significantly (P < 0·05) elevated in the group 24 h after injection of cloprostenol. There was good correlation between the in-vivo ovarian secretion rate and production rate during incubation in vitro for both inhibin (r = 0·57) and oestradiol (r = 0·60). When follicle diameter was compared with in-vitro hormone production there was good correlation for inhibin (r = 0·72) with larger follicles producing more inhibin, while the value for oestradiol was somewhat lower (r = 0·57) owing to the presence of large atretic follicles with low oestradiol production. Androstenedione production showed a lower correlation with follicle diameter (r = 0·39). When the four time periods were compared separately, there were significantly (P < 0·05) more follicles with high in-vitro oestradiol production (> 90 fmol/min) in the group at 36 h than in the other three groups, while inhibin release in relation to follicle size was similar in the four groups. Large oestrogenic follicles were responsible for 90% of the total oestradiol production during culture while only providing 55% of the total inhibin production, with large non-oestrogenic and small follicles contributing 33% and 12% of inhibin production respectively.

From the results of this study we conclude that while oestradiol is mainly produced by the large oestrogenic follicles, a considerable amount of inhibin is also produced by large non-oestrogenic and small follicles. We also found that a lack of variation in inhibin secretion rate in the intact animal was paralleled by a lack of variation in the pattern of inhibin produced from individual follicles.

Journal of Endocrinology (1992) 132, 225–234