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PubMed1988

Estrogen inhibits luteinizing hormone (LH), but not follicle-stimulating hormone secretion in hypophysectomized pituitary-grafted rats receiving pulsatile LH-releasing hormone infusions.

The differential feedback actions of estrogen (E2) on gonadotropin secretion were studied by means of an in vivo isolated pituitary paradigm. Adult female rats were hypophysectomized (hypox) and the next day received single anterior pituitary transplants (graft) under the kidney capsule. At the same time rats underwent bilateral ovariectomy. On the third day each animal was fitted with a catheter system which allowed for intermittent infusions of LHRH (250 ng/5 min.h) and chronic blood sampling. Rats received LHRH infusions for 7 days. On the sixth day of LHRH infusions blood samples were collected for 4 h 5, 15, 25, 35, 45 min after each hourly LHRH pulse. After 1 h of sampling, animals received sc injections of 2 micrograms estradiol benzoate (EB; n = 5) or oil vehicle (n = 5). Plasma LH, FSH, E2, and PRL levels in samples from all groups were determined by RIA. In hypox/graft rats LH release, but not FSH release, was pulsatile in response to the hourly LHRH infusions. Injection of EB in the hypox/graft rats significantly (P less than 0.05) suppressed LH release within 3 h by 57%, while FSH was unaffected. PRL levels were elevated by approximately 10-fold in the hypox/graft animals compared to those in pituitary-intact rats. These levels, however, were not changed as a function of steroid treatment and, therefore, could not account for the effects of EB on LH secretion. On the basis of these observations we conclude that 1) a major inhibitory effect of an acute injection of EB on LH secretion is exerted by a direct action on pituitary gonadotropes, and 2) E2 can differentially affect the release of LH and FSH by an intrapituitary mechanism. It is hoped that development of this model will allow for further investigation of the cellular mechanisms that mediate feedback actions of E2 on pituitary gonadotropes exposed to intermittent LHRH stimulation.

Animals↗

PubMed1989

Luteinizing hormone (LH)-releasing hormone: effects of induction of LH, follicle-stimulating hormone, and prolactin cell differentiation.

We investigated the influence of LHRH on the differentiation of gonadotrophs and lactotrophs in fetal pituitary glands transplanted beneath the renal capsules of adult hypophysectomized-orchidectomized hamsters (hosts). Hypophyses were removed from hamster fetuses at a gestational age of 14 days. Some of these were immediately fixed in Bouin's solution, and others were transplanted into the hosts. The hosts were injected sc twice daily with 1 microgram LHRH or vehicle for 16 days. Six hosts in each group were killed by decapitation 16 h after the last injection. Six 14-day-old normal male hamsters (age-matched to correspond to the age of the allografts at the time of the hosts' decapitation) also were decapitated. Sections of hypophyses in situ from fetal hamsters, from 14-day-old controls, and from allografts in each group were stained for LH, FSH, or PRL and with hematoxylin. No PRL-containing cells and very few LH or FSH cells (less than 0.025% of the adenohypophysial cell population) were observed in fetal pituitary glands. In allografts from the vehicle-treated hosts, 21.1% of adenohypophysial cells contained LH, but only 1.8% contained FSH. In allografts from LHRH-treated hosts, 28.0% and 22.9% of the adenohypophysial cells contained LH and FSH, respectively. Adenohypophyses that developed for the same length of time in situ had smaller percentages of adenohypophysial cells containing LH (23.8%) and FSH (15.5%) than the LHRH-treated group. LH-containing cells in allografts in the vehicle-treated hamsters, but not in the LHRH-treated animals, were reduced in size compared to those measured in situ. The number of lactotrophs in all allografted tissue was markedly reduced compared to that of lactotrophs in situ, and injection of LHRH into hamsters with allografts did not alter the percentage of adenohypophysial cells that were lactotrophs. These results suggest that in the hamster LHRH 1) plays an important role in stimulating the formation of immunoreactive FSH in the pituitary gland, 2) can increase the number of gonadotrophs that develop during the neonatal period, and 3) plays a role in controlling the size of gonadotrophs during development. The results also suggest that the development of lactotroph cell number requires close proximity to the hypothalamus and/or exposure to a neonatal environment. We found no evidence to support the view that LHRH, LH, or FSH stimulates immunoreactive lactotroph differentiation.

Animals↗

PubMed1990

Luteinizing hormone (LH)-releasing hormone: effects on maintenance of immunoreactive follicle-stimulating hormone and LH in adenohypophysial cells.

We investigated the importance of LHRH on the maintenance of FSH and LH immunoreactivity in gonadotrophs. Hypophysectomized orchidectomized hamsters (hosts) each received an allograft of a 7-week-old male hamster pituitary gland beneath their right renal capsule. Starting 6 days after transplantation, hosts were injected sc, twice daily with 1 micrograms LHRH or vehicle for 16 days. Twelve hosts in each group were killed by decapitation 16 h after the last injection. Allografts from six of the hamsters in each group and pituitary glands in situ from 10-week-old normal males were prepared for histological examination. Sections of tissue were stained for FSH or LH and with hematoxylin. Allografts from the remaining hamsters were homogenized to measure FSH and LH concentrations. In allografts from the vehicle-treated hosts, 22.8% of adenohypophysial cells stained for LH, while only 16.9% stained for FSH. In allografts from LHRH-treated hosts, 22.6% and 23.8% of the adenohypophyses cells stained for LH and FSH, respectively. Adenohypophyses that developed for the same length of time in situ had 24.8% and 24.1% of the cells staining for LH and FSH, respectively. Matching of some of the FSH and LH cells in serial flip-flopped sections of tissue from all hamsters revealed that many if not all gonadotrophs contained LH. LH- and FSH-containing cells in allografts were similar in size and shape, but were smaller and more circular in profile than those observed in situ. Treatment of hosts with LHRH did not alter gonadotroph size or shape, but it did reduce allograft LH concentration and elevate the serum FSH concentration compared to that in the vehicle-treated hamsters. These results suggest that in the hamster LHRH 1) plays a major role in maintaining FSH immunoreactivity in adenohypophysial tissue, 2) does not play a role in maintaining numbers of immunoreactive LH cells in adult adenohypophysial tissue, and 3) functions to maintain FSH synthesis at least in part in cells that contain LH.

Animals↗

PubMed1990

Luteinizing hormone (LH)-releasing hormone: chronic effects on LH and follicle-stimulating hormone cells and secretion in adult male rats.

We investigated whether chronic administration of LHRH to normal adult rats could increase the percentages of anterior pituitary gland (APG) cells that contain immunoreactive LH and/or FSH and gonadotropin secretion. Vehicle or 1 microgram LHRH was injected sc twice daily for 6 days, and rats were decapitated 16 h after the last injection. Treatment with LHRH caused nearly a doubling in the numerical density of LH and FSH cells and in the percentage of APG cells that contained LH or FSH. It also caused a shift in the gonadotroph population from LH and LH/FSH cells to LH/FSH cells. It did not change the mean size of gonadotrophs or APG weight. These changes at the light microscopic level were not accompanied by any apparent changes in LH cells at the ultrastructural level. However, they were accompanied by an approximate doubling of the basal serum LH and FSH concentrations, an increase in the APG FSH concentration, and an increase in the basal FSH release rate (measured in vitro). The results indicate that exogenous LHRH can be administered to increase numbers of gonadotrophs in the APG, synthesis of FSH in gonadotrophs, and basal serum LH and FSH concentrations.

Animals↗

PubMed1992

Inhibin suppresses luteinizing hormone (LH)-releasing hormone self-priming: direct action on follicle-stimulating hormone secretion and opposition of estradiol-enhanced LH secretion.

Previous studies have suggested that the ovary produces a factor that maintains the pituitary in a state of low LHRH responsiveness that must be overcome by the self-priming action of LHRH. To determine the role of inhibin in maintaining low LHRH responsiveness in pituitaries of diestrous female rats, endogenous inhibin was passively immunoneutralized in vivo, and the pituitaries were removed 18-20 h later and examined for LHRH responsiveness in vitro. Pituitaries from diestrous control rats produced the biphasic pattern of gonadotropin secretion that typifies LHRH self-priming: an initial low secretory response to LHRH (lag phase), followed by a protein synthesis-dependent transition to an enhanced rate of secretion with continued LHRH exposure (primed phase). Immunoneutralization of endogenous inhibin [antiserum (AS) treated] resulted in an increased rate of LH secretion during the lag phase, while no change was observed in the primed phase rate of LH secretion. FSH secretion from pituitaries of AS-treated rats was increased during the lag phase to a rate of secretion similar to that observed during the primed phase of FSH secretion from control pituitaries, and it was increased further during the primed phase of secretion. These results suggest that inhibin is at least partially responsible for the low secretion of LH observed during the lag phase response to LHRH exposure and is totally responsible for the lowered rate of FSH secretion during the lag phase. The observation that the enhanced rate of gonadotropin secretion observed with AS-treated pituitaries during the lag phase was resistant to inhibition of protein synthesis provides further evidence that a partial transition from the lag to the primed phase had already occurred. Pituitaries from ovariectomized rats were also examined in order to place the contribution of inhibin in perspective with the total ovarian influence on pituitary responsiveness to LHRH. Unexpectedly, LH secretion during the lag phase was similar to the low secretion rate of diestrous control pituitaries, and the higher primed rate of secretion failed to fully develop, suggesting that an additional ovarian factor was required to induce and maintain pituitary responsiveness to LHRH in terms of LH secretion. FSH secretion from the ovariectomized rats was similar to that observed from pituitaries of AS-treated rats, thus further supporting the concept that inhibin is fully responsible for the suppression of FSH secretion in response to LHRH. Plasma from the AS-treated rats revealed a 2-fold increase in estradiol levels compared with diestrous control rats.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1997

Effect of gonadotropin-releasing hormone (GnRH) pulse frequency on serum and pituitary concentrations of luteinizing hormone and follicle-stimulating hormone, GnRH receptors, and messenger ribonucleic acid for gonadotropin subunits in cows.

Thirty-two nutritionally anestrous cows were used to determine the effect of the frequency of exogenous GnRH pulses on ovarian follicular growth, serum concentrations of LH and FSH, and concentrations of LH, FSH, GnRH receptors (GnRH-R), messenger RNA (mRNA) for GnRH-R, and mRNA for gonadotropin subunits in the pituitary. Cows were randomly assigned to one of four treatments: 2 micrograms GnRH infused (i.v.) continuously during 1 h, 2 micrograms GnRH infused during 5 min once every hour, 2 micrograms GnRH infused during 5 min once every fourth hour, or saline (control) for 13 days. Infusion of GnRH every hour increased LH concentrations in serum (P < 0.05), but FSH concentrations were not affected by GnRH infusion. Luteal activity (LA) was assessed by the presence of corpora lutea and/or serum progesterone greater than 1 ng/ml. Six of eight cows infused with GnRH every hour had LA by day 13, whereas only 25% of cows infused either continuously or with a pulse every fourth hour had LA by day 13. None of the control cows had LA during the experiment (P < 0.01). Concentrations of LH and FSH in the pituitary were significantly reduced when GnRH was infused hourly or continuously. Concentrations of common alpha and FSH beta mRNA were not influenced by treatment. However, continuous infusion of GnRH decreased (P < 0.05) LH beta mRNA subunit. Concentrations of GnRH-R (P < 0.1) and GnRH-R mRNA (P < 0.05) were reduced when GnRH was infused continuously. We concluded that pulsatile secretion of LH is necessary for follicular growth and LA in beef cattle, and GnRH treatment differentially regulates LH and FSH gene transcription and serum concentrations of LH and FSH in cattle.

Animals↗

PubMed1998

Expression of growth hormone secretagogue-receptors by growth hormone-releasing hormone neurons in the mediobasal hypothalamus.

A novel class of synthetic compounds, termed GH-secretagogues (GHSs), have been shown to be potent stimulators of GH release, although their mechanism of action and functional significance remains obscure. The recent cloning of the rat GHS receptor (GHS-R) permitted the identification of numerous sites of expression of GHS-R in brain, but nothing is yet known about the cell types that express this receptor. We performed dual chromogenic and autoradiographic in situ hybridization to test the hypothesis that GHRH neurons in the hypothalamus coexpress GHS-R mRNA. GHS-R-hybridizing cells showed extensive overlap with GHRH-expressing neurons in both the arcuate (Arc) and ventromedial (VMN) hypothalamic nuclei. Quantification of the double-labeled cells revealed that approximately 27% of GHRH-hybridizing neurons in the Arc, and 22% of those in the VMN, expressed the GHS-R gene. These studies are the first to colocalize the GHS-R to any neurochemical cell type in rat brain. The results provide evidence that the GHSs may directly modulate GHRH release, and thereby stimulate GH secretion, through interaction with the GHS-R on hypothalamic GHRH mRNA-containing neurons.

Animals↗

PubMed2003

Nonsupplemented luteal phase characteristics after the administration of recombinant human chorionic gonadotropin, recombinant luteinizing hormone, or gonadotropin-releasing hormone (GnRH) agonist to induce final oocyte maturation in in vitro fertilization patients after ovarian stimulation with recombinant follicle-stimulating hormone and GnRH antagonist cotreatment.

Replacing GnRH agonist cotreatment for the prevention of a premature rise in LH during ovarian stimulation for in vitro fertilization (IVF) by the late follicular phase administration of GnRH antagonist may render supplementation of the luteal phase redundant, because of the known rapid recovery of pituitary function after antagonist cessation. This randomized two-center study was performed to compare nonsupplemented luteal phase characteristics after three different strategies for inducing final oocyte maturation. Forty patients underwent ovarian stimulation using recombinant (r-)FSH (150 IU/d, fixed) combined with a GnRH antagonist (antide; 1 mg/d) during the late follicular phase. When at least one follicle above 18 mm was observed, patients were randomized to induce oocyte maturation by a single injection of either r-human (h)CG (250 microg) (n = 11), r-LH (1 mg) (n = 13), or GnRH agonist (triptorelin; 0.2 mg) (n = 15). Retrieved oocytes were fertilized by either IVF or intracytoplasmatic sperm injection, depending on sperm quality. Embryo transfer was performed 3-4 d after oocyte retrieval. No luteal support was provided. Serum concentrations of FSH, LH, estradiol (E(2)), progesterone (P), and hCG were assessed at fixed intervals during the follicular and luteal phase. The median duration of the luteal phase was 13, 10, and 9 d for the r-hCG, the r-LH, and the GnRH agonist group, respectively (P = 0.005). The median area under the curve per day (from 4 d post randomization until the onset of menses) for LH was 0.50, 2.34, and 1.07 for the r-hCG, the r-LH, and the GnRH agonist group, respectively (P = 0.001). The median area under the curve per day for P was 269 vs. 41 and 16 for the r-hCG, the r-LH, and the GnRH agonist group, respectively (P < 0.001). Low pregnancy rates (overall, 7.5%; range, 0-18% per started cycle) were observed in all groups. In conclusion, the nonsupplemented luteal phase was insufficient in all three groups. In the patients receiving r-hCG, the luteal phase was less disturbed, compared with both other groups, presumably because of prolonged clearance of hCG from the circulation and the resulting extended support of the corpus luteum. Despite high P and E(2) concentrations during the early luteal phase in all three groups, luteolysis started prematurely, presumably because of excessive negative steroid feedback resulting in suppressed pituitary LH release. Hence, support of corpus luteum function remains mandatory after ovarian stimulation for IVF with GnRH antagonist cotreatment.

Adult↗

PubMed2004

Novel male hormonal contraceptive combinations: the hormonal and spermatogenic effects of testosterone and levonorgestrel combined with a 5alpha-reductase inhibitor or gonadotropin-releasing hormone antagonist.

We postulated that the addition of a combined types I and II, 5alpha-reductase inhibitor (dutasteride) or long-acting GnRH antagonist (acyline) to combination testosterone plus levonorgestrel treatment may be advantageous in the suppression of spermatogenesis for male contraception. This study aimed to examine effects of novel combination contraceptive regimens on serum gonadotropins and androgens and sperm concentration.This study was divided into three phases: screening (2 wk), treatment (8 wk), and recovery (4 wk). Twenty-two men (n = 5-6/group) received 8 wk of treatment with testosterone enanthate (TE, 100 mg im weekly) combined with one of the following: 1) levonorgestrel (LNG) 125 mug orally daily; 2) LNG 125 microg plus dutasteride 0.5 mg orally daily; 3) acyline 300 microg/kg sc every 2 wk (as a comparator for any additional progestin effects); or 4) LNG 125 microg orally daily plus acyline 300 microg/kg sc every 2 wk. Serum gonadotropin levels were similarly suppressed by all treatments, falling to a nadir between 1.2 and 3.4% and 0.5 and 0.8% baseline for FSH and LH, respectively (P < 0.05). Serum dihydrotestosterone levels were significantly (P < 0.05) decreased in the dutasteride group throughout the treatment period to a nadir of 31% baseline (wk 7). No significant differences in sperm concentrations among treatment groups were seen. Severe oligospermia (0.1-3 million/ml) or azoospermia was seen in none of five and four of five in TE + LNG; two of six and four of six in TE + LNG + dutasteride; two of six and four of six in TE + acyline; and one of five and three of five in TE + LNG + acyline groups, respectively. There was one nonresponder in each of the TE + LNG and TE + LNG + acyline groups.We conclude that the addition of a combined types I and II, 5alpha-reductase inhibitor or long-acting GnRH antagonist to a testosterone plus LNG regimen provides no additional suppression of gonadotropins or sperm concentration over an 8-wk treatment period. However, further evaluation of the effects of these regimens on the testis (including testicular steroid levels and germ cell maturation) and the treatment of larger numbers of men (and for longer periods) may provide data to support their place in contraceptive development.

Adult↗

PubMed2005

Growth hormone replacement is important for the restoration of parathyroid hormone sensitivity and improvement in bone metabolism in older adult growth hormone-deficient patients.

Alterations in PTH circadian rhythm and PTH target-organ sensitivity exist in adult GH-deficient (AGHD) patients and may underlie the pathogenesis of AGHD-related osteoporosis. GH replacement (GHR) results in increased bone mineral density, but its benefit in AGHD patients over 60 yr old has been debated. To examine the effect of age on changes in PTH circadian rhythm and target-organ sensitivity after GHR, we recruited 22 AGHD patients (12 were <60 yr of age, and 10 were >60 yr of age). Half-hourly blood samples were collected for PTH, calcium, phosphate, nephrogenous cAMP (marker of renal PTH activity), type-I collagenbeta C-telopeptide (bone resorption marker), and procollagen type-I amino-terminal propeptide (bone formation marker) before and after 1, 3, 6, and 12 months of treatment with GHR. Significant PTH circadian rhythms were present in both age groups throughout the study. After GHR, PTH decreased and nephrogenous cAMP, adjusted calcium, and bone turnover markers increased in both groups, suggesting increased PTH target-organ sensitivity. In younger patients, the changes were significant after 1 month of GHR, but, in older patients, the changes were delayed until 3 months, with maximal changes at 12 months. Older AGHD patients derive benefit from GHR in terms of improvement in PTH sensitivity and bone metabolism. Their response appears delayed and may explain why previous studies have not shown a positive effect of GHR on bone mineral density in older AGHD patients.

Adenoma↗

PubMed1973