A synthetic decapeptide analogue of human seminal plasma inhibin exhibiting specific suppression of follicle stimulating hormone release in rats

Synthesis and biological profile of a decapeptide analogue, [Tyr85, Cys(Acm)87]85-94 of human seminal plasma inhibin (HSPI) are described. The peptide suppressed the circulatory levels of follicle stimulating hormone (FSH) in adult male rats. No change in the levels of luteinizing hormone (LH) and prolactin (Prl) was observed. Whereas the peptide suppressed the release of both FSH and LH in vitro. This decapeptide is the smallest peptide reported so far to have FSH suppressing activity.     

Effect of gonadotropin-releasing hormone antagonists on serum follicle-stimulating hormone and luteinizing hormone under conditions of singular follicle-stimulating hormone secretion

Previous work has indicated that in long-term ovariectomized rats a potent antagonist to gonadotropin-releasing hormone (GnRH) suppressed serum luteinizing hormone (LH) more successfully than follicle-stimulating hormone (FSH). The present studies examined whether the rise in serum FSH which occurs acutely after ovariectomy, or during the proestrous secondary surge, depends on GnRH. In Experiment A, rats were ovariectomized at 0800 h of metestrus and injected with (Ac-dehydro-Pro1, pCl-D-Phe2, D-Trp3,6, NaMeLeu7)-GnRH (Antag-I) at 1200 h of the same day, or 2 or 5 days later. Antag-I blocked the LH response completely, but only partially suppressed serum FSH levels. Experiment B tested a higher dose of a more potent antagonist [( Ac-3-Pro1, pF-D-Phe2, D-Trp3,6]-GnRH; Antag-II) injected at the time of ovariectomy. The analog suppressed serum LH by 79% and FSH by 30%. Experiment C examined the effect of Antag-II on the day of proestrus on the spontaneous secondary surge of FSH, as well as on a secondary FSH surge which can be induced by exogenous LH. Antag-II, given at 1200 h proestrus, blocked ovulation and the LH surge expected at 1830 h, as well as increases in serum FSH which occur at 1830 h and at 0400 h. Exogenous LH triggered a rise in FSH in rats suppressed by Antag-II. In Experiment D proestrous rats were injected with Antag-II at 1200 h and ovariectomized at 1530 h. By 0400 h the antag had suppressed FSH in controls, but in the ovariectomized rats, a vigorous FSH response occurred.(ABSTRACT TRUNCATED AT 250 WORDS)     

Validation of the mechanisms proposed for the stimulatory and inhibitory effects of progesterone on gonadotropin secretion in the estrogen-primed rat: a possible role for adrenal steroids.

The stimulatory and inhibitory effects of progesterone on luteinizing hormone (LH) and follicle-stimulating hormone (FSH) secretion were found to be dependent on the length of estrogen exposure in ovariectomized estrogen-primed rats. Progesterone suppressed LH and FSH secretion when administered 16 hours after a single injection of estradiol to ovariectomized rats. If the estradiol treatment was extended over 40 hours by two injections of estradiol 24 hours apart, progesterone administration led to a highly significant elevation of both serum LH and FSH levels 6 hours later. In addition to the direct stimulatory effect on LH and FSH release, progesterone, when injected 1 hour before, was able to antagonize the suppressive effect of a third injection of estradiol on LH and FSH release. In the immature ovariectomized estrogen-primed rat, 10 IU of ACTH brought about a release of progesterone and corticosterone 15 minutes later and LH and FSH 6 hours later. Progesterone, but not corticosterone, appeared to be responsible for the effect of ACTH on gonadotropin release. The synthetic corticosteroid triamcinolone acetonide brought about LH and FSH release in the afternoon, while cortisol, similar to corticosterone, was unable to do so. Nevertheless, triamcinolone acetonide and cortisol brought about increased secretion of FSH the following morning.     

Changes in concentration of serum LH and FSH associated with estrogen-advanced ovulation in 4-day cyclic rats

Changes in concentration of serum luteinizing hormone (LH) and follicle stimulating hormone (FSH) associated with estrogen-advanced ovulation in 4-day cyclic rats were determined. 50 mcg of estradiol benzoate was administered sc on the 1st day of diestrus and LH and FSH were determined by radioimmunoassay 24, 29, and 47 hours postinjection. 48 hours postinjection, ovulation was determined by the presence of ova in the oviduct. Estradiol benzoate caused a significant (p less than .01) increase in serum LH after 24 and 29 hours and a drastic decrease after 47 hours postinjection. FSH increased (p less than .05) after 29 hours postinjection. These results suggest that an ovulatory gonadotropin surge occurs 24 hours ahead of schedule in estradiol-benzoate-treated rats.     

Effects of a potent antagonist to gonadotropin-releasing hormone on male rats: luteinizing hormone is suppressed more than follicle-stimulating hormone

Previous work with female rats showed that serum levels of follicle-stimulating hormone (FSH) are suppressed by gonadotropin-releasing hormone (GnRH) antagonists less than are levels of serum luteinizing hormone (LH), suggesting a lesser dependency of FSH on GnRH stimulation. The differential regulation of LH and FSH is known to have some aspects that are sexually asymmetrical, and it was of interest to see if males also show differential gonadotropin suppressibility after injection of an antagonist to GnRH. Male rats were prepared for serial sampling 4 wk after castration. After a blood sample was removed at Time Zero, [Ac-3-Pro1, pF-D-Phe2, -D-Trp3,6]-GnRH (Antag) was injected subcutaneously in oil; doses were 0, 4, 20, 100, 500, and 2500 micrograms. Blood was sampled at 2, 5, 12, 24 and 36 h postinjection. All doses above 4 micrograms had lowered LH levels by 2 h, and LH remained suppressed for 12 to 24 h at the three higher doses. By contrast, serum FSH was unaffected by any dose at 5 h, and was only marginally suppressed by the highest doses thereafter. As in females, therefore, FSH secretion in male rats appears not to be as dependent on GnRH as is LH secretion.     

Effects of luteinizing hormone on superovulatory and steroidogenic responses of rat ovaries to infusion with follicle-stimulating hormone

Immature female rats were infused s.c. continuously over a 60-h period with a partially purified porcine pituitary follicle-stimulating hormone (FSH) preparation having FSH activity 4.2 x NIH-FSH-S1 and luteinizing hormone (LH) activity 0.022 x NIH-LH-S1. High rates of superovulation were observed in rats receiving 1 U FSH/day, with 69 +/- 11 oocytes/rat recovered as cumulus-enclosed oocytes from oviducts on Day 1 (equivalent to the day of estrus). Addition of LH to the FSH, at dosages equivalent to 2.5-100 micrograms/day NIH-LH-S1 equivalents (2.5-100 mU) resulted in a dose-related inhibition of superovulation, reaching a nadir of 15 +/- 7 oocytes recovered from rats receiving 50 mU LH/day together with 1 U FSH/day. At the two highest LH doses, 50 and 100 mU/day, ovulation was advanced so that 12 +/- 3 and 15 +/- 4 oocytes, respectively, were recovered from oviducts of these rats flushed on the morning of Day 0, compared to none in rats infused with FSH alone. Ovarian steroid concentrations (ng/mg) observed on the morning of Day 0 in rats infused with FSH alone were progesterone, 0.50 +/- 0.13; testosterone, 0.16 +/- 0.08; androstenedione, 0.06; and estradiol, 0.23 +/- 0.05. On the morning of Day 1, ovarian progesterone concentrations in rats infused with FSH alone had risen to 3.30 +/- 0.33 ng/mg, whereas concentrations of testosterone, androstenedione, and estradiol, had fallen to essentially undetectable levels. Addition of LH to the FSH infusion resulted in dose-related increases, on Day 0, of all four steroids up to a dosage of 25 mU LH/day. At higher LH dosages, Day 0 ovarian concentrations of androgens and estradiol fell markedly, while progesterone concentrations continued to increase. Histological examination of ovaries revealed increases in the extent of luteinization of granulosa cells in follicles with retained oocytes on both Days 0 and 1 in rats infused with 25 and 50 mU LH/day together with 1 U FSH/day, compared to those observed in rats receiving FSH alone. These findings indicate that the elevated progesterone levels on Day 0 and inhibition of ovulation observed at these LH doses were due to premature luteinization of follicles, thus preventing ovulation. At lower LH doses, no sign (based on histologic or steroidogenic criteria) of premature luteinization was evident, suggesting that the decreased superovulation in these rats was due to decreased follicular maturation and/or increased atresia rather than to luteinization of follicles without ovulation.(ABSTRACT TRUNCATED AT 400 WORDS)     

Differential actions of GnRH and rat hypothalamic extracts in release of hypophysial FSH and LH in vitro.

A study was made of the separate patterns of luteinizing hormone (LH) and follicle stimulating hormone (FSH) release from isolated rat pituitary tissue evoked by synthetic gonadotropin releasing hormone (GnRH) or female hypothalamic extracts (HE), respectively, in a continuous perifusion system. Under defined conditions, gonadotropin release from hemipituitaries was relatively stable and reproducible. Absolute levels of LH and FSH release evoked by HE in terms of their GnRH content were always greater than those following exposure to synthetic GnRH at varying doses. Synthetic GnRH released more FSH than LH. In contrast, the HE released slightly higher levels of LH than FSH. The data suggest that the female rat hypothalamus contains substances other than GnRH, capable of releasing both LH and FSH. It is possible that such unidentified components can modify the hypophysial action of GnRH, resulting in particular circumstances in a differential release of LH and FSH.     

Neonatal release of gonadotropins is essential for development of ovarian follicle-stimulating hormone receptors

In the rat, ovarian follicle-stimulating hormone (FSH) receptors increase markedly during the first two postnatal weeks, when serum gonadotropin levels are most elevated. This study was conducted to evaluate the hypothesis that these high gonadotropin levels, and in particular FSH, are involved in the acquisition of FSH receptors by the developing ovary. Gonadotropin release was suppressed by administration of several non-aromatizable androgens, among which dihydrotestosterone propionate (DHTP) was the most effective. In one series of experiments the steroids were administered from Days 5 to 11, and serum FSH and luteinizing hormone (LH) were measured on Day 12. Surprisingly, FSH receptor content was greater in rats with suppressed serum gonadotropins than in controls. The greatest increase in available receptors was observed in DHTP-treated rats in which serum FSH was reduced to 20% of control values and LH suppressed to undetectable values. DHTP failed to directly increase available FSH receptors in hypophysectomized immature rats. Magnesium chloride (MgCl2) treatment of ovarian membranes removed bound 125I-hFSH by 87% without affecting receptor viability. Exposure of control 12-day-old ovaries to MgCl2 increased available FSH receptors to a level similar to that of ovaries from DHTP-treated rats not exposed to MgCl2, suggesting that more receptors were available in DHTP-treated rats because serum FSH was suppressed. Earlier initation of DHTP treatment (postnatal Day 1) suppressed serum FSH and LH to undetectable values by Day 5 and decreased FSH receptor content below control values by Day 12. MgCl2 treatment only slightly increased available receptors in these DHTP-treated animals.(ABSTRACT TRUNCATED AT 250 WORDS)     

Bone loss in ovariectomized rats: dominant role for estrogen but apparently not for FSH

Estrogen deficiency as the sole factor underlying post‐menopausal osteoporosis was challenged, in light of reports that both follicular stimulation hormone (FSH) receptor and FSHβ knockout mice were resistant to bone loss, suggesting a detrimental role for FSH. We assessed whether lowering FSH levels by gonadotropin realizing (GnRH) analog decapeptyl in ovariectomized female rats (OVX) affects bone. Wistar‐derived 25 days old OVX female rats were injected for 10 weeks with estradiol‐17β (E₂), with GnRH analog (decapeptyl) or with both. FSH and luteinizing hormone (LH) serum levels were markedly increased in OVX rats, with smaller growth plates with disrupted architecture; heavy infiltration of bone marrow with numerous adipocytes and reduced thickness of cortical bone. In OVX rats treated with E₂, FSH, and LH levels were intermediate, the tibia was similar to that of intact rats, but there was reduced thickness of cortical bone. In decapeptyl treated OVX rats, FSH and LH levels were suppressed, the organization of growth plate and the trabecular bone were disrupted, and there were fewer proliferative and chondroblastic cells and a large adipocytes population in bone marrow, but an increased trabecular bone volume (TBV). In the E₂ + decapeptyl treatment, FSH and LH levels were suppressed, with partially restored growth plate architecture and improved TBV. In conclusion, E₂ deficiency is the dominant factor impairing bone loss in OVX and concomitant changes in FSH/LH levels achieved by decapeptyl have some modulating, though complex role in this setting. The role of high FSH levels in post‐menopausal bone loss requires further investigation using combined sub‐optimal doses of the different hormones. J. Cell. Biochem. 112: 128–137, 2011. © 2010 Wiley‐Liss, Inc.     

Dissociation of copulation from ovulation in pregnant rabbits

Experiments were designed to determine why copulation in the pregnant rabbit does not terminate pregnancy while treatment with ovulatory doses of luteinizing hormone (LH) human chorionic gonadotropin (hCG) or luteinizing hormone-releasing hormone (LHRH) is known to do so. Pregnant rabbits (Day 8) were mated or were injected with hCG (25 IU/doe) or LHRH (1, 10 micrograms/kg). Serial blood samples were collected over the next 72 h and analyzed for content of LH, follicle-stimulating hormone (FSH) and progesterone. At sacrifice, uteri and ovaries from these animals were examined for viability of the embryos and for signs of recent ovulation. Injection of hCG or LHRH into pregnant animals led to ovulation and to patterns of LH, FSH and progesterone secretion like those which precede ovulation in estrous rabbits. However, mating the pregnant does did not lead to ovulation or to any changes in the circulating hormones. To investigate whether the elevated levels of progesterone during pregnancy were responsible for the dissociation of coitus from ovulation, nonpregnant rabbits were injected with progesterone (2 mg/kg) and then mated or injected with hCG or LHRH. In virtually every respect, the numbers of ovulations and the patterns of hormone secretion in the progesterone-treated, nonpregnant rabbits mimicked those observed in the 8-day pregnant animals; injection of hCG or LHRH caused ovulation and hormonal surges while hCG caused ovulation only. Mating did not lead to ovulation or any change in blood levels of LH, FSH or progesterone. Taken together, the results show that the elevated circulating levels of progesterone, characteristic of pregnancy, are probably responsible for the dissociation of copulation from gonadotropin release in pregnant rabbits.     

Selective release of follicle-stimulating hormone and luteinizing hormone by 5 alpha-dihydroprogesterone and 3 alpha, 5 alpha-tetrahydroprogesterone in pregnant mare's serum gonadotropin-primed immature rats exposed to constant light

The effects of 5 alpha-dihydroprogesterone (5 alpha-DHP) and 3 alpha, 5 alpha-tetrahydroprogesterone (3 alpha, 5 alpha-THP) on follicle-stimulating hormone (FSH) and luteinizing hormone (LH) release were examined in the pregnant mare's serum gonadotropin (PMSG)-primed immature female rat (8 IU PMSG at 28 days of age) maintained in constant light. Control rats kept in 14L:10D conditions exhibited proestrous-like surges of LH and FSH release with peak levels attained at 1800 h on the second day after PMSG treatment. In rats exposed to constant light, the PMSG-induced surges of LH and FSH were not only delayed until 1000 h on the third day after PMSG, resulting in a delay in ovulation, but were also significantly attenuated when compared to the gonadotropin surges that occurred on Day 2 in rats kept under normal light-dark conditions. The administration of 5 alpha-DHP significantly enhanced the release of FSH at 1000 h on Day 3 when compared to constant light-exposed controls, but had no effect on LH. Treatment with 3 alpha, 5 alpha-THP selectively potentiated the release of LH at 1000 h on Day 3 and had an attenuating effect on FSH release on Days 2 and 3. These observations confirm earlier findings in the immature ovariectomized estrogen-primed rat and suggest that 5 alpha-DHP and 3 alpha, 5 alpha-THP may have significant roles in the regulation of FSH and LH secretion.     

The effects of porcine follicular fluid inhibin on gonadotropin secretion in the rabbit

Porcine follicular fluid (pff), treated with charcoal to remove steroids, was used to determine whether inhibin is active in the laboratory rabbit. When pff (5 ml/4 kg body weight) was injected (ip) into does that had been castrated 2 weeks earlier, there was a significant decline in blood follicle-stimulating hormone (FSH) levels; the decline lasted for 8-12 h. Blood levels of luteinizing hormone (LH) were suppressed, but only briefly at 3 h after injection. In other experiments, intact does which had been injected with pff 9 h and 10 min before receiving a single, i.v. injection of luteinizing hormone-releasing hormone (LHRH) (10 micrograms/kg body weight) showed a sharp reduction in the concentration of LH in the blood samples collected 15, 30 and 60 min after LHRH administration. Secretion of FSH responded poorly to LHRH stimulation, and pff had little suppressive action on blood levels. Having established that the pff preparation had inhibin activity, its action on the postovulatory surge of FSH secretion was next examined. This release of FSH, which occurs 6 to 36 h after ovulation, has been hypothesized to be required for the establishment of pregnancy by stimulating the growth of the ovarian follicles supplying the luteotropic estradiol. To test this hypothesis, pff was injected into rabbits every 8 h for the first 5 days of pregnancy and found to block the postovulatory FSH surge. The patterns of secretion of LH and progesterone in the same pff-injected animals were, however, not altered from normal pregnancy patterns by pff.(ABSTRACT TRUNCATED AT 250 WORDS)     

Central effects of an antagonist and an antiserum to substance P on serum gonadotropin and prolactin secretion

The central effects of both an antagonist and an antiserum to substance P (SP) on gonadotropin and prolactin (Prl) secretion were studied in castrated male rats. The lateral ventricular injection (20 micrograms) of an analogue to SP possessing antagonistic properties resulted in significantly suppressed serum LH levels without altering serum FSH and Prl levels when compared with saline-injected control animals. Similarly, the lateral ventricular injection of an antiserum to SP also resulted in significantly suppressed LH levels when compared to control animals injected with normal rabbit serum. Additionally, no changes were observed in the levels of serum FSH and Prl as a result of the anti-SP injection. Thus, although indirect, these results support the hypothesis that SP may have a central stimulatory action on LH secretion, but not FSH and Prl secretion.     

Testosterone selectively increases serum follicle-stimulating hormonal (FSH) but not luteinizing hormone (LH) in gonadotropin-releasing hormone antagonist-treated male rats: evidence for differential regulation of LH and FSH secretion

Both testosterone (T) and gonadotropin-releasing hormone (GnRH)-antagonist (GnRH-A) when given alone lower serum luteinizing hormone (LH) and follicle-stimulating hormone (FSH) in intact and castrated rats. However, when graded doses of testosterone enanthate (T.E.) were given to GnRH-A-treated intact male rats, a paradoxical dose-dependent increase in serum FSH occurred; whereas serum LH remained suppressed. This surprising finding led us to ask whether the paradoxical increase in serum FSH in GnRH-A-suppressed animals was a direct stimulatory effect of T on the hypothalamic-pituitary axis or the result of a T effect on a testicular regulator of FSH. To test these hypotheses, we treated adult male castrated rats with GnRH-A and graded doses of T.E. In both intact and castrated rats, serum LH remained undetectable in GnRH-A-treated rats with or without T.E. However, addition of T.E. to GnRH-A led to a dose-dependent increase in serum FSH in castrated animals as well, thus pointing against mediation by a selective testicular regulator of FSH. These data provide evidence that pituitary LH and FSH responses may be differentially regulated under certain conditions. When the action of GnRH is blocked (such as in GnRH-A-treated animals), T directly and selectively increases pituitary FSH secretion.     

Luteinizing Hormone and Follicle Stimulating Hormone-Releasing Hormone Test in Patients with Hypothalamic Pituitary-Gonadal Dysfunction

A standard intravenous 100 μg luteinizing hormone/follicle stimulating hormone-releasing hormone (LH/FSH-RH) test was used to assess the pituitary gonadotrophin responses in 155 patients with a variety of diseases of the hypothalamic-pituitary-gonadal axis. In all but nine patients there was an increase in circulating levels of either LH or FSH in response to the releasing hormone though 137 (88%) were clinically hypogonadal. It was not possible with this test to distinguish between hypothalamic and pituitary causes of hypogonadotrophic hypogonadism, since a variety of LH and FSH responses emerged within the disease groups. However, primary gonadal failure characteristically resulted in exaggerated gonadotrophin response. The potential therapeutic use of the gonadotrophin releasing decapeptide is suggested in certain patients with hypogonadotrophic hypogonadism.     

Luteinizing hormone-independent luteinization and ovulation in the hypophysectomized rat: a possible role for the oocyte?

Immature hypophysectomized, estrogen-treated rats were used to study the regulation of luteinization. Particular attention was focused on the potential role of the oocyte in this process. Rats were injected for 2 days with follicle-stimulating hormone (FSH) to stimulate follicular development. Within 48 h following FSH treatment, many follicles became luteinized, as determined by morphometric analysis. This luteinization occurred in the absence of detectable levels of luteinizing hormone (LH). The number of follicles undergoing luteinization was dependent on the FSH dose. In addition, ovulation occurred in some of the animals receiving the highest doses of FSH (3-micrograms or 5-micrograms injections). The majority of follicles undergoing luteinization or ovulation were greater than 400 microns in diameter. Luteinized follicles exhibited positive reactivity for cholesterol side-chain cleavage enzyme, 3 beta-hydroxysteroid dehydrogenase, lipid, and alkaline phosphatase, which was similar to that found in corpora lutea of the cycle. Serum progesterone (P0) and 20 alpha-hydroxypregn-4-en-one levels were elevated in animals with luteinized follicles, especially in those animals that also underwent ovulation. Morphological evaluation of oocytes showed that the majority of luteinized follicles contained a degenerating oocyte. Oocyte degeneration was highly correlated (r = 0.94) to luteinization. These results demonstrate that luteinization and ovulation can occur in the FSH/estrogen-primed hypophysectomized rats in the absence of detectable serum LH. Furthermore, LH-independent luteinization was strongly correlated to degenerative changes in the oocyte. These results provide new evidence to support the concept that the oocyte may be an intraovarian regulator of luteinization.     

Bimodal effects of luteinizing hormone and role of androgens in modifying superovulatory responses of rats to infusion with purified porcine follicle-stimulating hormone

Prepubertal (28-30 days old) female rats were infused s.c. over a 60-h period with a purified porcine pituitary follicle-stimulating hormone (FSH) preparation having FSH specific activity 8.4 times that of NIH-FSH-S1 and luteinizing hormone (LH) specific activity less than 0.005 times that of NIH-LH-S1, based on radioreceptor assays. When the FSH infusion rate of this preparation was increased over the range of 0.5-2 units/day (mg NIH-FSH-S1 equivalent), an all-or-none response was observed, with the threshold dose for superovulation being between 1 and 2 units/day. Eleven of twelve rats receiving the 2 units/day dose ovulated a mean +/- SEM of 67 +/- 8 oocytes on the morning of the third day after the beginning of FSH infusion. Addition of human chorionic gonadotrophin (hCG), as a source of LH activity, to a subthreshold (1 U/day) FSH infusion rate resulted in 20% of rats ovulating at an hCG dosage of 50 mIU/day; increasing the hCG infusion to 200 mIU/day concomitant with the subthreshold FSH infusion rate increased ovulation rate to a mean of 69 +/- 8/rat, with 100% of rats ovulating. To determine the effect of varying both FSH infusion rates and LH:FSH ratios, FSH was infused at several rates, with hCG added to give varying hCG:FSH ratios for each FSH infusion rate. Administration of hCG alone was ineffective in causing ovulation except at the highest infusion rates. Adding hCG to FSH to reach a ratio of 0.2 IU hCG/U FSH significantly increased the superovulatory response to an intermediate, 1 U/day FSH dose, but not to the low, 0.5 U/day dose.(ABSTRACT TRUNCATED AT 250 WORDS)     

Modulation of pituitary responsiveness to LHRH by androgens in ovariectomized female rats.

The effect of androgens on pituitary response to luteinizing-hormore-releasing hormone (LHRH) and their ability to modify effects of 17beta-estradiol (E2) on pituitary responsiveness to LHRH were tested in ovariectomized rats maintained on a daily dose of 0.25 microgram estradiol benzoate per rat for 6 d before androgen administration. Testosterone propionate (TP) (4, 40, 400, or 4000 microgram per rat), administered 24 h before LHRH (500 ng per rat), had no significant effect on luteinizing hormone (LH) or follicle-stimulating hormone (FSH) response. Similar doses of dihydrotestosterone (DHT) did not significantly alter the LH response but significantly suppressed the FSH response. Even the lowest dose completely blocked the FSH response to LHRH. TP in combination with 4 or 400 microgram of E2 suppressed the stimulatory effect of E2 on both LH and FSH response to LHRH in a dose-related manner. DHT and E2 in combination affected LH response inconsistently, whereas their ratio determined FSH response; there was pronounced inhibition of FSH response in rats given high doses of DHT combined with low doses of E2; DHT inhibition of FSH response in animals receiving 4 microgram of DHT with 400 microgram E2 was partially overcome by the stimulatory effect of E2. Our results indicate that TP and DHT affect LH and FSH response to LHRH differently. The ratio of androgen to estrogen is important in determining the response to LHRH.     

The effect of mating on the afternoon of proestrus on serum LH (and FSH) and ovulation in the rat

Possible relationships between coitus and serum gonadotrophin levels and ovulation in the rat were investigated. Female rats were mated betw een 1700 and 1730 or between 1800 and 1830 hours. 1.3 ml of blood was withdrawn by cardiac puncture 30 minutes postcoitus for luteinizing hormone (LH) analysis. After autopsy on the morning of estrus, counts were made of tubal ova, and LH and follicle-stimulating hormone (FSH) were measured in terminal blood from all animals. Those mated at 1700-1730 with no cardiac puncture showed significantly more ova than those with cardiac puncture (p less than .05) and those which were neither mated nor received cardiac puncture (p les than .05). No differences were found between those mated at 1800-1830 hours because of the large variance in each group. Coitus during the time of normal mating did not increase LH levels 30 minutes postmating or terminal LH and FSH levels. Terminal LH levels were significantly increased in the no cardiac puncture-no mate animals (p less than .05) in comparison with the cardiac puncture-no mate animals.     

Gonadotrophin concentrations and ovulation rates in Suffolk ewes actively or passively immunized against inhibin alpha

Mature Suffolk ewes were either actively or passively immunized against the synthetic fragment of porcine inhibin alpha, pI alpha(1-30), to determine the effects on gonadotrophin secretion and ovulation rate. Thirteen control ewes were immunized against human serum albumin, 12 ewes were actively immunized against pI alpha(1-30) and 36 ewes were passively immunized with pI alpha(1-30) antiserum. Blood samples were collected at 4-h intervals for 72 h from oestrus-synchronized ewes following the withdrawal of the progestagen pessaries. Mean gonadotrophin concentrations measured during the oestrous cycle of control ewes, ewes actively immunized against pI alpha(1-30) and ewes passively immunized against pI alpha(1-30) were similar, but their secretory profiles differed. Serum concentrations of follicle-stimulating hormone (FSH) were highest in ewes which had received antiserum at the time of pessary withdrawal; FSH concentrations did not decrease during the follicular phase of the oestrous cycle in ewes given antiserum 24 h after pessary withdrawal. Subtle but significant increments in serum FSH concentrations were observed in all passively immunized ewes in which sampling commenced at the time of treatment. The amplitude of the preovulatory luteinizing hormone (LH) peak, but not of the FSH peak, and the postovulatory secondary rise in FSH were lower (P less than 0.05) in actively immunized ewes than in control ewes. The mean (+/- s.e.) ovulation rate for actively immunized ewes (6.6 +/- 1.0) was 3 times higher (P less than 0.05) than that for control ewes (2.0 +/- 0.2), but was unaffected by passive immunization (range, 1.8-2.3).(ABSTRACT TRUNCATED AT 250 WORDS)