Attenuated In Vivo Progesterone Secretion by Ovine Corpora Lutea After Exposure to Luteinizing Hormone

1989 ◽  
pp. 399-402
Author(s):  
Ov Slayden ◽  
Fredrick Stormshak
1974 ◽  
Vol 61 (3) ◽  
pp. 455-463 ◽  
Author(s):  
R. M. MOOR

SUMMARY The object of this study was to test the hypothesis that levels of luteinizing hormone (LH), comparable to those circulating at oestrus, inhibit oestrogen secretion from Graafian follicles of sheep. Three experimental approaches were used. Follicles maintained in organ culture secreted high levels of oestrogen into the medium throughout a 7-day culture period; almost no progesterone was secreted under such conditions. By contrast, oestrogen secretion declined precipitously and progesterone secretion increased rapidly after the addition of LH (0·25 μg–10 μg NIH-LH-S 17/ml) to the culture medium. In experiments combining in-vivo and in-vitro techniques, follicles were obtained from sheep from which the corpora lutea had been removed 24 h previously. The large follicles explanted from these sheep secreted high levels of oestrogen throughout the 7 days in culture. Insignificant amounts of oestrogen were, however, secreted in culture by large follicles that had been explanted from sheep in which 1 mg LH had been infused between 18 and 24 h after removal of the corpus luteum. Experiments carried out entirely in vivo showed that intravenous infusion of 1 mg LH into sheep from which the corpora lutea had been removed 18 h previously prevented the ovaries from secreting, during the ensuing 22 h, the large amounts of oestrogen they would otherwise have produced. The results demonstrate that oestrogen secretion by large Graafian follicles is terminated both in vitro and in vivo by an amount of LH corresponding to that released at oestrus.


1991 ◽  
Vol 69 (9) ◽  
pp. 1288-1293 ◽  
Author(s):  
Yallampalli Chandrasekhar ◽  
David T. Armstrong

Serum and ovarian progesterone levels and in vitro production of progesterone by preovulatory follicles were measured on proestrus in pregnant mare's serum gonadotropin (PMSG) primed immature rats in which the luteinizing hormone (LH) surge and ovulation were blocked by administration of the antiandrogen hydroxyflutamide. Serum progesterone levels observed at 12:00 on proestrus were significantly elevated, twofold above those observed in vehicle-treated controls, by in vivo administration of 5 mg hydroxyflutamide 4 h earlier. In control rats, proestrous progesterone did not increase until 16:00, in parallel with rising LH levels of the LH surge. No LH surge occurred in the hydroxyflutamide-treated rats, ovulation was blocked, and serum progesterone declined throughout the afternoon of proestrus, from the elevated levels present at 12:00. Administration of human chorionic gonadotropin (hCG) at 11:00 advanced the elevation of serum progesterone by 2 h in vehicle-treated controls and prevented the decline in progesterone levels in hydroxyfiutamide-treated rats. The patterns of change in ovarian tissue concentrations with time and treatment were essentially similar to those observed for serum progesterone. In in vitro experiments, progesterone secretion during 24 h culture of preovulatory follicles obtained on PMSG-induced proestrus was significantly increased, sixfold, by addition to the culture media of 370 μM but not of 37 μM hydroxyflutamide. Testosterone (50 nM) and hCG (20 mIU/mL) caused 26- and 14-fold increases, respectively, in progesterone secretion by cultured follicles. Hydroxyflutamide significantly reduced the stimulatory effect of testosterone but not of hCG on progesterone secretion in vitro. These results suggest that the antiandrogen hydroxyflutamide stimulates progesterone secretion, both in vivo and in vitro, through an initial androgen-agonistic action, before its antagonistic action is expressed. Its androgen-antagonistic action is responsible for its ability to inhibit testosterone-induced progesterone secretion in vitro. Its failure to reduce hCG-stimulated progesterone secretion in vivo and in vitro indicates that the latter stimulation is exerted independently of, and not as a consequence of, androgen action. The decrease in serum progesterone levels on the afternoon of proestrus therefore appears to be a consequence rather than a cause of the absence of an LH surge in the hydroxyflutamide-treated rats. It is concluded that the inhibitory effect of hydroxyflutamide on the preovulatory LH surge and ovulation is due not to inhibition of progesterone secretion at the ovarian level but most likely to neuroendocrine site(s) of action of the inhibitor.Key words: antiandrogen, hydroxyflutamide, progesterone, luteinizing hormone, ovulation, human chorionic gonadotropin.


1973 ◽  
Vol 57 (1) ◽  
pp. 63-74 ◽  
Author(s):  
I. ROTHCHILD ◽  
R. B. BILLIAR ◽  
I. T. KLINE ◽  
G. PEPE

SUMMARY To test the hypothesis of Raj & Moudgal (1970) that luteinizing hormone (LH) is the essential luteotrophin during pregnancy in the rat, pregnant rats were hypophysectomized and hysterectomized on either day 12 or day 15 of pregnancy, and the changes in peripheral serum progesterone level measured. The serum progesterone level remained at approximately the day-12 value for 3 days after hypophysectomy and hysterectomy on day 12, but fell drastically and remained low after the same operation on day 15, or in pseudopregnant rats operated on on day 12, or after removal of the ovaries from pregnant rats on day 12. Oestrogen treatment increased the serum progesterone level slightly in the pregnant rats after hypophysectomy and hysterectomy, but not after ovariectomy; it had no effect in the pseudopregnant rats, with or without deciduomata, or in lactating rats nursing litters of seven to nine pups. The corpora lutea stopped growing or slowly regressed soon after hypophysectomy—hysterectomy in all except the pregnant rats operated on on day 12 and treated with oestrogen, and in these growth was very slight. The luteal content of progesterone did not change for 3 days after hypophysectomy—hysterectomy on day 12 of pregnancy, and fell slightly thereafter. The metabolic clearance rate of progesterone was not significantly changed by hypophysectomy—hysterectomy. It thus appears that true secretion of progesterone continues in pregnant rats for about 3 days after day 12 in the absence of the pituitary and placentas, but at a much lower rate than that found in intact, or in day-12 hypophysectomized pregnant rats (Pepe & Rothchild, 1972a). The placental luteotrophin thus seems to increase the rate of progesterone secretion in the absence of LH. The results do not seem to fit with the hypothesis that LH is essential for progesterone secretion.


Reproduction ◽  
2005 ◽  
Vol 129 (1) ◽  
pp. 61-73 ◽  
Author(s):  
T A Bramley ◽  
D Stirling ◽  
G S Menzies ◽  
D T Baird

Seasonally anoestrous Welsh Mountain ewes received 250 ng gonadotrophin-releasing hormone (GnRH) every 2 h, with (Group 1;n= 13) or without (Group 2;n= 14) progesterone priming for 48 h. Fourteen control ewes (Group 3) were studied during the luteal phase in the breeding season. Animals in Group 4 (n= 12) received progesterone priming followed by 250 ng GnRH at increasing frequency for 72 h, while ewes in Group 5 (n= 13) were given three bolus injections of 30 μg GnRH at 90-min intervals. All treatment regimens induced ovulation. However, only corpora lutea (CL) from ewes in Group 3 (breeding season) or Group 4 exhibited normal luteal function. Luteal luteinizing hormone (LH) receptor levels were significantly higher on day 12 than day 4, and CL from groups with adequate CL (3 and 4) had significantly higher125I-human chorionic gonadotrophin (hCG)-binding levels than the three groups with inadequate CL on day 12. LH-binding affinity was unchanged. Exogenous ovine LH (10 μg)in vivoon days 3 or 11 after ovulation induced a pulse of progesterone in ewes with adequate CL: however, ewes in Groups 1, 2 and 5 showed no significant response. Basal progesterone secretionin vitrowas significantly greater on day 4 than on day 12. Maximal steroidogenic responses of adequate and inadequate CL to hCG and to dibutyryl cyclic-3′,5′-AMP were similar at both stages of the luteal phase. However, the EC50for hCG on days 4 and 12 was 10-fold lower for groups with an adequate CL (0.1 IU hCG/ml) than for inadequate-CL groups (1 IU hCG/ml;P<0.05). Thus, in addition to the well-characterized premature sensitivity of GnRH-induced inadequate CL to endometrial luteolysin, we have shown (1) a marked decrease in total number of cells in the CL, a profound reduction in vascular surface area, and a decrease in mean large luteal cell volume (with no change in large luteal cell numbers), (2) decreased luteal LH receptor and progesterone content compared with adequate CL and (3) that CL that were becoming, or were destined to become, inadequate failed to respond to ovine LHin vivoand were 10-fold less sensitive to hCG in terms of luteal progesterone secretionin vitro.


1995 ◽  
Vol 133 (6) ◽  
pp. 701-717 ◽  
Author(s):  
Bernd Hinney ◽  
Christina Henze ◽  
Wolfgang Wuttke

Hinney B, Henze C, Wuttke W. Regulation of luteal function by luteinizing hormone and prolactin at different times of the luteal phase. Eur J Endocrinol 1995;133:701–17. ISSN 0804–4643 In 54 healthy women luteal function was assessed by sequential withdrawals of blood samples at 10-min intervals for 8–10 h. Subgroups of the women were studied during the early and late ovulatory period and during the early, mid- and late luteal phase. Bio- and immunoreactive luteinizing hormone (LH), prolactin, testosterone, estradiol and progesterone levels were determined in each sample. While the bio- and immunoreactivity of LH pulses correlated fairly well, a number of bio- or immunoreactive LH pulses were observed that were not detected by the respective other method. Responsivity of the corpus luteum to LH episodes developed during the second half of the luteal phase and was most marked in cases where LH episodes were accompanied by prolactin episodes. In the absence of prolactin episodes, LH episodes did not stimulate progesterone or estradiol secretion. The highest incidence of coincident LH and prolactin pulses was observed during the mid- and late luteal phase. Serum testosterone levels showed also some fluctuations but these were independent of immuno- or bioactive LH episodes and therefore most likely not of luteal origin. Prior to menstruation LH episodes were not any more stimulatory to progesterone secretion, indicating that it is not the withdrawal of LH but, rather, another possibly intraovarian mechanism that results in luteolysis. In a number of women, increased estradiol and progesterone secretion was strictly related to the prior occurrence of LH and prolactin pulses. In other subjects, both gonadal steroids fluctuated largely with no discernible correlation to LH fluctuations. This may indicate that in these subjects the corpora lutea have some degree of autonomous regulation. W Wuttke, Abteilung für Klinische und Experimentelle Endokrinologie, Universitäts-Frauenklinik, Robert-Koch-Strasse 40, D-37075 Gottingen, Germany


1977 ◽  
Vol 72 (3) ◽  
pp. 379-383 ◽  
Author(s):  
K. M. HENDERSON ◽  
R. J. SCARAMUZZI ◽  
D. T. BAIRD

SUMMARY Corpora lutea of ewes bearing ovarian autotransplants were infused for 4 h with prostaglandin F2α (PGF2α) (10 μg/h), PGF2α + PGE2 (10 μg/h of each), PGE2 (10 μg/h) or saline on day 10 of the cycle. Ovarian venous blood obtained before, during, and up to 12 h after the infusion period, was assayed for progesterone. Prostaglandin F2α produced an immediate, rapid and sustained decline in progesterone secretion, but infusion of PGE2 together with PGF2α prevented the decline until after the infusion. Progesterone secretion was unaffected by infusion of PGE2 alone. Oestrous behaviour was observed in four out of seven animals infused with PGF2α but in only one out of six infused with PGF2α + PGE2. None of the animals infused with PGE2 alone or saline only came into heat.


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