Role of luteinizing hormone in luteotropic complex of pregnant hamster

1987 ◽  
Vol 252 (4) ◽  
pp. E500-E504 ◽  
Author(s):  
H. Tamura ◽  
G. S. Greenwald

Hamsters were hypophysectomized on day 4 of pregnancy (day 1 = sperm in vaginal smear) and injected subcutaneously on days 4-7 with various combinations of 200 micrograms prolactin (Prl), 10 micrograms follicle-stimulating hormone (FSH), and 20 micrograms luteinizing hormone (LH) in polyvinylpyrrolidone (PVP) to decrease its rate of absorption or in saline. End points for luteal function on day 8 were maintenance of pregnancy, serum progesterone (P4), luteal weight, and luteal binding for human chorionic gonadotropin, FSH, and Prl. After hypophysectomy, a drastic decline occurred in all parameters including an 89% decrease in luteal weight. Injection of Prl did not maintain pregnancy nor serum P4 but partially maintained luteal weight and human chorionic gonadotropin binding sites per corpus luteum. The minimal luteotropic complex of Prl and FSH was effective in maintaining pregnancy and significantly increased serum P4 and Prl and FSH receptors but not to control levels; Prl and LH (PVP) was also effective to the same extent. Antral follicles were lacking after either treatment. The effects of FSH cannot be attributed to LH contamination. All variables were restored to control levels by Prl plus FSH plus LH (PVP) and antral follicles were present; Prl plus FSH plus LH (saline), however, induced luteolysis and reduced most values to the levels found in untreated, hypophysectomized animals. Thus, the luteotropic activity of LH was only demonstrable when it was injected in a long-acting form; when delivered as a bolus, LH (saline) was luteolytic.

2020 ◽  
Vol 103 (6) ◽  
pp. 1217-1228
Author(s):  
Victor E Gomez-León ◽  
João Paulo Andrade ◽  
Brian W Kirkpatrick ◽  
Sadrollah Molaei Moghbeli ◽  
Alvaro García-Guerra ◽  
...  

Abstract Studying selection of multiple dominant follicles (DFs) in monovulatory species can advance our understanding of mechanisms regulating selection of single or multiple DFs. Carriers of the bovine high fecundity Trio allele select multiple DFs, whereas half-sib noncarriers select a single DF. This study compared follicle selection during endogenous gonadotropin pulses versus during ablation of pulses with Acyline (GnRH antagonist) and luteinizing hormone (LH) action replaced with nonpulsatile human chorionic gonadotropin (hCG) treatment in Trio carriers (n = 28) versus noncarriers (n = 32). On Day 1.5 (Day 0 = ovulation), heifers were randomized: (1) Control, untreated; (2) Acyline, two i.m. doses (Days 1.5 and D3) of 3 μg/kg; (3) hCG, single i.m. dose of 50 IU hCG on Day 1.5 followed by daily doses of 100 IU; and (4) Acyline + hCG. Treatments with nonpulsatile hCG were designed to replace LH action in heifers treated with Acyline. Acyline treatment resulted in cessation of follicle growth on Day 3 with smaller (P < 0.0001) maximum follicle diameter in Trio carriers (6.6 ± 0.2 mm) than noncarriers (8.7 ± 0.4 mm). Replacement of LH action (hCG) reestablished follicle diameter deviation and maximum diameter of DFs in both genotypes (8.9 ± 0.3 mm and 13.1 ± 0.5 mm; P < 0.0001). Circulating follicle stimulating hormone (FSH) was greater in Acyline-treated than in controls. Finally, Acyline + hCG decreased (P < 0.0001) the number of DFs from 2.7 ± 0.2 to 1.3 ± 0.2 in Trio carriers, with most heifers having only one DF. This demonstrates the necessity for LH in acquisition of dominance in Trio carriers (~6.5 mm) and noncarriers (~8.5 mm) and provides evidence for a role of GnRH-induced FSH/LH pulses in selection of multiple DFs in Trio carriers and possibly other physiologic situations with increased ovulation rate.


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.


1984 ◽  
Vol 247 (1) ◽  
pp. E84-E87
Author(s):  
P. K. Westfahl ◽  
L. E. Horton ◽  
H. L. Stadelman ◽  
J. A. Resko

The manner in which exogenous 17 beta-estradiol (E2) induces premature luteolysis in primates is unclear. In an effort to determine whether exogenous luteotropic hormone inhibits E2-induced luteolysis, E2 capsules were implanted subcutaneously in 11 cynomolgus macaques during the early luteal phase; six animals received injections of human chorionic gonadotropin (hCG; 7.5, 10, or 15 IU/day) for 10 days, and the remaining monkeys received saline. Blood was collected once daily for measurement of E2, progesterone, and bioactive luteinizing hormone (LH). Peak progesterone concentrations were between 0.7 and 5.0 ng/ml and declined prematurely in monkeys given E2 plus saline; the luteal phase was 11.5 +/- 0.6 days (mean +/- SE). With E2 plus hCG treatment, serum progesterone continued to increase after E2 capsule placement and reached peak levels of 4.0-13.0 ng/ml; the luteal phase was 15.3 +/- 0.5 days. Therefore, E2-induced luteolysis was overcome by concurrent administration of hCG. These results suggest that exogenous tropic hormone circumvents the inhibitory influence of E2 on luteal function, but the details of the interaction remain unknown.


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