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PubMed1984

Effects of pulsatile infusion of luteinizing hormone-releasing hormone on luteinizing hormone secretion and ovarian function in hypophysial stalk-transected beef heifers.

Hypothalamic regulation of luteinizing hormone (LH) secretion and ovarian function were investigated in beef heifers by infusing LH-releasing hormone (LHRH) in a pulsatile manner (1 microgram/ml; 1 ml during 1 min every h) into the external jugular vein of 10 hypophysial stalk-transected (HST) animals. The heifers were HST approximately 30 mo earlier. All heifers had increased ovarian size during the LHRH infusion. The maximum ovarian size (16 +/- 2.7 cm3) was greater (P less than 0.01) than the initial ovarian size (8 +/- 1.4 cm3). Ovarian follicular growth occurred in 4 of 10 HST heifers in response to pulsatile LHRH infusion. In 2 heifers, an ovarian follicle developed to preovulatory size, but ovulation occurred in only 1 animal after the frequency of LHRH was increased (1 microgram every 20 min during 8 h). In blood samples obtained at 20-min intervals every 5th day, LH concentrations in peripheral serum remained consistently low (0.9 ng/ml) and nonepisodic in the 10 HST heifers during infusion of vehicle on the day before beginning LHRH. In 7 of 10 HST animals, episodic LH secretion occurred in response to pulsatile infusion of LHRH. In 3 of these long-term HST heifers, however, serum LH remained at basal levels and the isolated pituitary seemingly was unresponsive to pulsatile infusion of LHRH as indicated by sequential patterns of gonadotropin secretion obtained at 5-day intervals. These results indicate that pulsatile infusion of LHRH induces LH release in HST beef heifers.

Animals↗
PubMed1985

Changes in luteinizing hormone-releasing hormone content of discrete hypothalamic areas associated with spontaneous and induced preovulatory luteinizing hormone surges in the domestic hen.

It is widely assumed that luteinizing hormone-releasing hormone (LHRH) neuronal activation is involved in the preovulatory surge of LH in the hen. In addition, this LH surge may be initiated by ovarian progesterone (P4) release. Thus, spontaneous and P4-induced LH surges should be associated with acute changes in LHRH content of discrete hypothalamic areas associated with LHRH cell bodies and/or LHRH axon terminals. Medial preoptic area (mPOA) and infundibulum (INF) LHRH content was measured by radioimmunoassay at intervals before, at, and following peak LH levels of a spontaneous preovulatory surge of LH, as well as when this surge was advanced by P4 administration in laying hens. Nonlaying birds served as additional controls. Levels of serum LH, P4, 17 beta-estradiol and pituitary LH were also measured. Increased (P less than 0.05) LHRH content in mPOA without changes in the INF are associated with peak serum LH levels of the spontaneous LH surge. By contrast, decreased (P less than 0.05) LHRH content in both mPOA and INF is associated with peak serum LH levels when the spontaneous surge was advanced 8 h by P4 administration to laying hens. Medial preoptic area and INF LHRH contents were significantly lower (P less than 0.05) in nonlaying than in laying hens.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Hypothalamic deafferentation and luteinizing hormone-releasing hormone effects on secretion of luteinizing hormone in prepubertal pigs.

The control of luteinizing hormone (LH) secretion was investigated in ovariectomized, prepubertal Yorkshire pigs by comparing the effects of anterior (AHD), complete (CHD), and posterior (PHD) hypothalamic deafferentation to sham-operated controls (SOC). Gilts (n = 16) were assigned randomly to treatments, fitted with an indwelling jugular catheter, and ovariectomized 2 days before deafferentation or sham-operation (Day 0). Blood for radioimmunoassay (RIA) of LH was collected sequentially at 20-min intervals for a period of 2 h before and 24, 48, 72, and 96 h after hypothalamic deafferentation or SOC. Episodic LH release after AHD or CHD was abolished (p less than 0.01), but not after PHD or SOC. Concentrations of serum LH in AHD and CHD dropped (p less than 0.01) at 24 and 48 h after surgery. Levels of LH before and after surgery in PHD and SOC were similar (p greater than 0.05). Infusion of 25 micrograms LH-releasing hormone (LHRH) i.v. at 72 and 96 h after hypothalamic deafferentation and SOC increased (p less than 0.01) serum LH to peak levels within 15 min. after infusion; LH returned to basal levels 60-80 min later. By 96 h after surgery, LH response to LH-releasing hormone (LHRH) was less in AHD and CHD as compared with the response at 72 h postinjection. Concentrations of LH in PHD and SOC were similar (p greater than 0.05) at 72 and 96 h, respectively. The results from this study clearly indicate that neural stimuli originating or traversing the neural areas rostral to the median eminence are required for secretion of LH in the pig.(ABSTRACT TRUNCATED AT 250 WORDS)

Afferent Pathways↗
PubMed1987

Ovine luteinizing hormone. I. Effects of castration and steroid administration on the charge heterogeneity of pituitary luteinizing hormone.

Chromatofocusing was used to separate and characterize the isohormones of ovine luteinizing hormone (oLH) in the pituitaries of rams, wethers, and wethers receiving Silastic implants containing 5 alpha-dihydrotestosterone (DHT), 17 beta-estradiol (E2), or DHT plus E2. Extracts of anterior pituitaries were prepared by homogenization and centrifugation at 100,000 X g. Castration reduced the amount of oLH in the pituitary, even though peripheral levels were elevated. Pituitary oLH concentrations in wethers were further reduced by all three steroid treatments. When subjected to chromatofocusing on pH 10.5 to 7.0 gradients, pituitary extracts yielded eight peaks of immunoreactive oLH, which eluted with apparent isoelectric points of greater than 9.8, 9.26, 9.14, 9.07, 8.98, 8.91, and less than or equal to 7.0. These isohormones were designated A-G and Z, respectively. In rams, isohormones F and G were the predominant species, representing approximately equal to 57% of the immunoreactive oLH recovered from the column. Castration resulted in a subtle shift toward more basic isohormones. DHT administration caused an increase in the relative amount of isohormone A, whereas E2 treatment resulted in an increase in isohormone Z. DHT and E2 in combination produced increases in the relative amounts of both isohormones A and Z. All eight oLH isohormones were active in an in vitro LH bioassay and exhibited biological-to-immunological-assay (B/I) ratios in the ram ranging from 0.4 to 2.8. Isohormone F exhibited the highest B/I ratio in all the treatment groups. Similarly, isohormone F was clearly the predominant biologically active form of oLH in all groups. These results demonstrate that at least eight immunoreactive and biologically active forms of pituitary oLH can be separated by using chromatofocusing; the pattern of oLH isohormones is markedly different from that in the rat; castration has a minimal effect on the pattern of oLH isohormones in pituitary extracts; and exogenous gonadal steroid administration reduces the amount of oLH in the pituitary and changes the pattern of oLH isohormones, resulting in a higher percentage of less biologically active forms.

Animals↗
PubMed1991

Comparison of the steroidogenic response of luteinized granulosa cells from rhesus monkeys to luteinizing hormone and chorionic gonadotropin.

The dynamics of the steroidogenic response of nonprimate gonadal cells to gonadotropins suggests that the biologic action of pituitary LH differs from that of placental CG. To compare the response to LH and CG in primate species, luteinized granulosa cells (LGCs) obtained from rhesus monkeys following follicle stimulation were cultured in vitro. The pattern and levels of progesterone (P) produced during culture was influenced by the concentration (0-10%) and type (fetal bovine or macaque) of serum in the medium and whether LGCs were plated on plastic or extracellular matrix from bovine corneal endothelial cells. After 2-3 days of culture, LGCs were exposed acutely (15-30 min) or chronically (6 h) to 1 or 100 ng/ml human LH (hLH, NIH 1-2) or hCG (CR123), 50 micrograms/ml ovine LH (oLH, NIH-oLH-25), or incubated in the absence of gonadotropins (controls). After the first 15-30 min, the media were changed at 30-min intervals. Both acute and chronic exposure to hLH, hCG, and oLH increased (p less than 0.05) P concentrations above control levels within 15-30 min. There were no differences in the patterns or levels of P elicited by hLH or hCG over time for each treatment condition. Chronic exposure to 1 and 100 ng/ml hLH or hCG and 50 micrograms/ml oLH sustained P levels above that of controls for the 6-h interval. Acute exposure to 1 ng/ml hLH or hCG failed to maintain elevated P levels throughout the experiment.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Effect of naloxone and luteinizing hormone releasing hormone pulses on plasma luteinizing hormone concentration in ewe lambs.

A study was conducted to determine the effect of pulses of naloxone on plasma LH concentration in prepubertal ewes and to see if this treatment affects the pituitary response to subsequent LHRH pulses. Prepubertal ewes (n = 5) received three intracarotidal pulses of naloxone (NAL, 1 mg/kg BW) and four pulses of Luteinizing Hormone Releasing Hormone (LHRH, 1 micrograms/pulse) at hourly intervals. Control ewes (n = 5) received saline instead of NAL followed by the LHRH pulses at the same frequency. Blood samples were collected from one hour before the first pulse of saline or NAL at 15 min intervals for four hours and at 30 min intervals for another four hours. Plasma LH concentration was measured by radioimmunoassay. The first pulse of NAL increased plasma LH levels compared to the basal levels and compared to control animals (P less than 0.01). The succeeding pulses were ineffective. LHRH provoked an increase in plasma LH concentration in control as well as in treated animals but the amplitude of the net peak height increased progressively up to the third pulse in NAL treated animals, while there was no increase in pituitary responsiveness to LHRH in control prepubertal ewes. Also, the area under the LHRH response curve was greater (P less than 0.05) in animals pretreated with NAL than in lambs pretreated with saline. The results suggest that there is an inhibitory opioid tone over LH secretion in female lambs. NAL increases the responsiveness to exogenous LHRH pulses, probably as a result of endogenous LHRH release.

Animals↗
PubMed1990

Facilitatory role of neuropeptide Y on the onset of puberty: effect of immunoneutralization of neuropeptide Y on the release of luteinizing hormone and luteinizing-hormone-releasing hormone.

To examine the role of neuropeptide Y (NPY) in the first luteinizing hormone (LH) surge of puberty, the effect of passive immunoneutralization of NPY with antiserum against NPY (anti-NPY) injected centrally (third ventricle) or peripherally (jugular vein) was studied in pubertal female rats on the day of first proestrus. Both peripheral and central anti-NPY administration reduced the magnitude of the LH surge during the afternoon of first proestrus; however, the central route of administration appeared to be most effective. Centrally administered anti-NPY also reduced the magnitude of proestrous LH-releasing hormone (LHRH) release into pituitary portal blood in these rats. These results suggest that endogenous NPY plays a facilitatory role in the generation of the LHRH surge necessary for preovulatory gonadotropin release and puberty.

Animals↗
PubMed1991

Effect on luteinizing hormone secretion of GABA receptor modulation in the medial preoptic area at the time of proestrous luteinizing hormone surge.

Using a bilateral medial preoptic area (MPOA) infusion system in conscious female rats we have investigated the role of the GABA system in this area on the proestrous luteinizing hormone (LH) surge. Fifteen-minute blood samples for LH estimation were taken throughout the afternoon of proestrus from female rats exhibiting 4-day oestrous cycles and implanted at least 2 weeks prior with cerebral guide cannulae. Between 15:00 and 17:00 h rats received an infusion (1 microliter/30 min) of artificial cerebrospinal fluid (n = 7), 10 microM GABA (n = 6) or 10 microM bicuculline methiodide (BMI, n = 6). Animals infused with GABA failed to exhibit an LH surge, while BMI-treated animals displayed an LH surge which was not significantly different to controls. These data show that on the afternoon of proestrus, there are no tonic modulatory actions of the GABA system, acting through the GABAA receptor, on neural elements controlling the LH surge in the MPOA. If, however, GABA levels are elevated in the MPOA at this time then the LH surge is blocked. In conjunction with data from correlative studies showing a decrease in endogenous GABA release prior to the LH surge, we suggest that this fall in activity is an essential component of the LH surge mechanism.

Animals↗
PubMed1997

Regulation of gonadotropin-releasing hormone and luteinizing hormone secretion by AMPA receptors. Evidence for a physiological role of AMPA receptors in the steroid-induced luteinizing hormone surge.

Recent work has demonstrated that glutamate functions as a major transmitter involved in the regulation of gonadotropin-releasing hormone (GnRH) and luteinizing hormone (LH) secretion in female animals, although the specific receptors and mechanisms mediating its effects have not been completely worked out. The purpose of the present study, therefore, was to examine the role of the AMPA (alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid)-type glutamate receptor in the control of GnRH and LH secretion in female animals. Toward this end, the dose- and steroid-dependent effects of AMPA on GnRH and LH secretion in female rats were investigated using both in vitro and in vivo approaches, and the role of AMPA receptors in the production of the steroid-induced LH surge was also assessed. The results of the study revealed that central administration of AMPA resulted in a stimulation of LH release in the estrogen-primed ovariectomized adult rat. AMPA was also found to potently stimulate GnRH release in vitro from mediobasal hypothalamic (MBH) fragments obtained from estrogen-primed ovariectomized adult rats, and this effect was blocked by the selective AMPA receptor antagonist, NBQX. The mechanism of action of AMPA appeared to differ from that of N-methyl-D-aspartate (NMDA) as AMPA, in contrast to NMDA, failed to elevate nitric oxide synthase activity in the hypothalamus. The effect of AMPA on LH secretion was demonstrated to be steroid dependent, as central administration of AMPA stimulated LH release in estrogen-primed ovariectomized rats, but was inhibitory to LH release in non-estrogen-primed ovariectomized rats. In contrast, AMPA stimulated GnRH release equally well from MBH fragments obtained from estrogen-primed or non-estrogen-primed ovariectomized rats. The different effects of AMPA on LH release may be due to different pituitary sensitivities between the two models, or alternatively, AMPA may stimulate the release of LH inhibitory factors in the ovariectomized rat in the absence of estrogen. Finally, a physiological role for AMPA receptors in the production of the steroid-induced LH surge was suggested, based on the finding that central administration of the selective AMPA receptor antagonist, NBQX, into the third cerebroventricle significantly attenuated the steroid-induced LH surge in the ovariectomized adult female rat.

Animals↗
PubMed1986

Correlative study on sex differences in pituitary luteinizing hormone content and the number of immunoreactive luteinizing hormone cells in perinatal rats.

Sex differences in both pituitary luteinizing hormone (LH) content and the number of LH cells were correlatively studied in perinatal male and female rats. In the fetal pituitaries of late gestation, no sex difference was observed. On the day of birth, LH content and LH cell numbers were significantly greater in female than in male rats. Both of the two sex differences became more pronounced during the 1st and 4th postnatal days. Hormone synthesis and proliferation of pituitary LH cells are probably suppressed by testicular steroids in perinatal male rats.

Animals↗
PubMed1987

Pulsatile release of bioactive luteinizing hormone in prepubertal girls: discordance with immunoreactive luteinizing hormone pulses.

An assessment of pulsatile secretion of luteinizing hormone (LH), measured by both immunoassay (I-LH) and rat interstitial cell testosterone production bioassay (B-LH), as well as of follicle-stimulating hormone and glycoprotein hormone alpha-subunit was carried out in seven normal prepubertal and six normal premenarcheal pubertal girls. Samples were obtained at 20-min intervals for a 6-h period. The hormone secretion profiles were analyzed by several computerized methods yielding pulse frequency and amplitude, interpulse basal levels, and percentage increments, with bio/immuno ratios calculated for peak and basal concentrations. In these prepubertal girls, mean B-LH levels were 12% of I-LH, with B/I ratio of 0.13; 30% of samples were below assay sensitivity (0.10 mIU/ml) for B-LH, but all I-LH (1.25 mIU/ml) were detectable. In the pubertal group, B-LH levels were 30% of I-LH, with mean B/I ratio of 0.24 and undetectable B-LH in 29% of samples. Pulsatile secretion in prepubertal girls was found in five of seven (1/150 min) for B-LH and six of seven (1/212 min) for I-LH; only two of six pubertal girls had detectable pulses. Discordance of B- and I-LH pulses were frequent, with 56% of B-LH pulses lacking an I-LH pulse and 47% of I-LH pulses not having a B-LH pulse. These data demonstrate that both B- and I-LH are secreted episodically in prepubertal girls; I-LH-like material is present in higher concentrations than B-LH in these girls; and substantial discordance of B- and I-LH pulses exist.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1977

Relationship between luteinizing hormone releasing hormone concentration in hypophysial portal blood and luteinizing hormone release in intact, castrated, and electrochemically-stimulated rats.

The concentration of luteinizing hormone releasing hormone (LHRH) in hypophysial portal plasma was determined in pentobarbital anesthetized,intact and castrated rats of both sexes, including proestrous rats following electrochemical stimulation of the medial preoptic area (MPOA). Mean LHRH levels in portal plasma obtained between 1400--1700 h from estrous and diestrous rats and from rats ovariectomized for 8 weeks were similar and ranged from 50--55 pg/ml, but the LHRH levels in proestrous rats were less than 12 pg/ml. In addition, hypophysial portal plasma collected during 1100 to 1400 h from animals orchidectomized for 8 weeks and from intact male rats contained mean LHRH concentrations that ranged from 50--65 pg/ml and 30--35 pg/ml, respectively. Electrochemical stimulation of the MPOA in the female rat on the afternoon of proestrus resulted in a marked increase in the concentration of LHRH in portal plasma. LHRH levels in portal plasma during the 0 to 30, 30 to 60, 60 to 90, 90 to 120, and 120 to 150-min periods after electrochemical stimulation of the MPOA were 105 +/- 24.2, 61 +/- 10.8, 51 +/- 8.2, 36 +/- 5.3, and 32 +/- 4.1 pg/ml, respectively. LHRH levels in portal plasma from the unstimulated rats were not detectable (less than 12 pg/ml) in most of the animals. In another group of proestrous rats, the effect of rabbit anti-LHRH serum or normal rabbit serum (NRS) on the release of LH after electrochemical stimulation of MPOA was examined. Pretreatment of proestrous rats with anti-LHRH serum blocked the release of LH due to MPOA stimulation, whereas pretreatment with NRS did not inhibit LH release. On the basis of these findings, it is concluded that electro-chemical stimulation of the MPOA in proestrous rats increases LHRH levels in portal blood and that the enhanced secretion of LHRH stimulates the release of LH from the pituitary gland.

Animals↗
PubMed1976

Effect of active and passive immunization with luteinizing hormone-releasing hormone on serum luteinizing hormone and follicle-stimulating hormone levels and the ultrastructure of the pituitary gonadotrophs in castrated male rats.

The effect of active and passive immunization with luteinizing hormone-releasing hormone (LHRH) on serum LH and follicle-stimulating hormone (FSH) levels and the ultrastructure of the pituitary gonadotrophs was investigated in castrated male rats. Two weeks after castration, the animals were immunized with Glu1-LHRH conjugated with human serum albumin (hSA), immunized with hSA only, or left uninjected. Immunogens were administered every 2 weeks. Four weeks after the initiation of immunization with hSA-Glu1-LHRH, 2 out of 4 rats showed parallel decreases in serum LH and FSH levels associated with a rise of serum antibody titer to LHRH. Serum LH and FSH levels remained suppressed throughout the experiment in these rats. On the other hand, both LH and FSH levels in hSA-immunized rats or non-immunized rats remained elevated, and typical castration cells containing large vacuoles were found in the pituitary. Although castration cells existed in the pituitary of rats which produced antibody to LHRH by active immunization, these cells were markedly degranulated, and secretory granules were scarce in the cytoplasm. In another experiment, rats were injected iv with one ml sheep anti-LHRH gamma-globulin (anti-LHRH) or normal sheep gamma-globulin (NSG) every 2 days for 3 weeks, starting one day after castration, when serum LH and FSH levels were already elevated. All the animals which received anti-LHRH showed a decrease in both serum LH and FSH levels, which remained low throughout the study, in a range comparable to those in intact normal male rats. On the other hand, in the animals which received NSG, both LH and FSH levels remained high or increased further throughout the experiment, and the pituitary contained numerous castration cells. Castration cells were completely absent from the pituitaries of rats treated with anti-LHRH, suggesting that castration cells are formed as a result of increased secretion of LHRH. Some FSH gonadotrophs in these castrated rats were atrophic. It was difficult to distinguish the LH gonadotrophs in rats which were either actively or passively immunized with LHRH; however, they seem not to have contributed significantly to the development of castration cells. In any case, antibody to the LHRH decapeptide drastically affected both LH and FSH cells, providing additional evidence for the concept that LHRH represents the physiological LHRH and FSHRH.

Animals↗
PubMed1983

Clomiphene citrate induces luteinizing hormone release through hypothalamic luteinizing hormone-releasing hormone in vitro.

The releasing effects of clomiphene citrate (clomiphene) on luteinizing hormone (LH) and LH-releasing hormone (LRH) were examined in a sequential double chamber superfusion system by superfusing the mediobasal hypothalami (MBH) and/or pituitaries excised from normal female rats in dioestrus. When the MBH and the pituitary were superfused in sequence with medium containing 2 X 10(-10) M oestradiol (E2), two significant peaks in LH release (60-130% increase, P less than 0.05) were observed 40 min and 90 min after the administration of 3 X 10(-8) mol clomiphene. Administration of clomiphene in medium without E2 induced a low peak (25-50% increase, P less than 0.05) of LH released from the pituitary perfused in series with the MBH. Administration of clomiphene did not cause a marked increase of LH from the pituitary superfused alone, when superfused with or without E2 containing medium. The concentration of LRH in the efflux was significantly increased (50-100%) 40 min and 90 min after clomiphene administration when MBH was superfused with medium containing E2, whereas clomiphene had no effect when superfused with medium alone. These data indicate: 1) that clomiphene induces LRH release from the MBH, that it may induce LH release, in part, by acting directly at the pituitary level; 2) that changes in LH after clomiphene administration coincide with LRH release, and 3) that a certain concentration of E2 may be necessary for the secretion of LRH by clomiphene.

Animals↗
PubMed1984

Prolonged combined in vivo pre-treatment with luteinizing hormone-releasing hormone (LRH) and oestradiol benzoate causes long-lasting suppression of the autonomous and the LRH-stimulated secretion of luteinizing hormone and follicle stimulating hormone. An in vitro study.

The effect of a combined in vivo pre-treatment with luteinizing hormone-releasing hormone (LRH) and oestradiol benzoate (EB) on the autonomous and the 'supra-maximally' LRH-stimulated in vitro release of LH and FSH by pituitary glands of 2 weeks ovariectomized (OVX) rats was studied using a perifusion system. The concentration of LRH in the perifusion medium was 1 microgram/ml. Pre-treatment with LRH during 6 days was effected by means of sc implanted Alzet osmotic minipumps (MP). Control rats received a piece of silastic with the dimensions of a minipump ('sham-pump'; Sh-P). EB, 3 micrograms/injection or solvent (arachis oil) was sc injected on days-3 and -1 (day of perifusion: day 0). Of the pituitary glands of EB-injected, Sh-P-implanted rats both the autonomous and the LRH-stimulated secretion of LH and the LRH-stimulated secretion of FSH were significantly higher than those of the oil-injected, Sh-P-implanted rats without EB administration. Pretreatment with LRH for 6 days had a suppressing effect on the autonomous and the LRH-induced depletion of the pituitary LH and FSH stores. In combination with EB, the suppressing effect of LRH pre-treatment on the LRH-stimulated secretion of LH and FSH was still greater: the pituitary gland appeared to be fixed in a relatively unresponsive state with very low autonomous LH and FSH secretion. It is discussed that increase of pituitary LRH-responsiveness due to EB demands withdrawal of the pituitary gland from the influence of LRH, an effect which is in vivo achieved by the negative feedback of oestrogen on the hypothalamus.

Animals↗
PubMed1994

Inhibition of luteinizing hormone, follicle-stimulating hormone and sex-steroid levels in men and women with a potent antagonist analog of luteinizing hormone-releasing hormone, Cetrorelix (SB-75).

Cetrorelix (SB-75; [Ac-D-Nal(2)1, D-Phe(4Cl)2, D-Pal(3)3, D-Cit6, D-Ala10] luteinizing hormone-releasing hormone (LHRH)) is a new highly potent antagonist analog of LHRH containing the D-ureidoalkyl amino acid D-citrulline at position 6 and is free of allergenic effects. This study shows the inhibition of LH and follicle-stimulating hormone (FSH) release in normal men, postmenopausal women and patients with gonadal dysgenesis, using different doses and i.m., s.c. and i.v. routes of administration of SB-75. The mean serum levels of LH and FSH in normal men who received one single dose of 300 micrograms of SB-75 sc started to decline rapidly 1 h after its administration; the LH suppression was sustained for 14 h and that of FSH up to 24 h or longer as the samples were obtained only up to this time. The nadir for LH was reached at 14 h and that for FSH at 24 h or later after administration of the antagonist (p < 0.05). Serum levels of total and free testosterone decreased after the first hour and this inhibition was maintained for up to 14 h. The nadir for total testosterone was at 6 h and that for free testosterone was at 8 h (p < 0.001), corresponding to 56% and 60% of inhibition, respectively. In postmenopausal women, inhibition of the elevated basal serum LH and FSH levels occurred after a single injection of the antagonist analog SB-75 in doses of 75, 150, 300, 600 and 1200 micrograms using im, sc and iv routes of administration.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Inhibitory effects of a luteinizing-hormone-releasing hormone agonist implant on ovine fetal gonadotrophin secretion and pituitary sensitivity to luteinizing-hormone-releasing hormone.

Sheep fetuses at day 70 of gestation (term = 145 days) were implanted subcutaneously with a biodegradable implant containing a luteinizing-hormone-releasing hormone (LHRH) agonist (buserelin) to investigate whether treatment with LHRH agonist would induce a state of desensitization of the fetal gonadotrophs and thus influence fetal gonadal development. Treatment with the LHRH agonist for 35-40 days caused a significant reduction in mean fetal plasma concentrations of LH and follicle-stimulating hormone (FSH) compared with control fetuses. LH pulses were evident in control fetuses but were completely abolished by buserelin treatment. Furthermore, the pituitary content of LH and FSH was significantly depleted in fetuses implanted with LHRH agonist. A bolus intravenous injection of 500 ng LHRH given to control fetuses caused a rapid and significant increase in plasma LH and FSH concentrations which was sustained for at least 60 min after injection. Pretreatment with buserelin completely abolished the LH and FSH responses to a bolus injection of LHRH. There were no differences between the sexes in fetal gonadotrophin concentrations or pituitary sensitivity to LHRH in control or agonist-treated fetuses. Furthermore, buserelin treatment for 35-40 days had no effect on the morphological appearance of the fetal gonads when compared with control fetuses, at least to day 110 of pregnancy. These results provide evidence for the induction of a state of desensitization of the LHRH receptors of the fetal pituitary gonadotrophs following long-term treatment with an LHRH agonist, but provide no evidence for a role for gonadotrophin secretion in gonadal development at this stage in fetal life.

Analysis of Variance↗
PubMed1976

Application of an in-vitro perifusion technique to studies of luteinizing hormone release by rat anterior hemi-pituitaries: Self-potentiation by luteinizing hormone releasing hormone.

A technique is described for the continuous perifusion of rat adenophypophyses. Exposure of the perifused glands to repeated equal 5 min stimuli with hypothalamic extract resulted in a series of equal peaks of corticotrophin secretion, the response was proportional to log dose over the range 0 - 25-2 - 0 rat hypothalamic equivalents/ml. Repeated equal stimuli with hypothalamic extract, or with luteinizing hormone releasing hormone (LH-RH) at concentrations of 2 or 10 ng/ml, resulted in a progressively increasing series of peaks of LH secretion, i.e. a self-potentiating or priming effect. The effect took between 30 min and 1 h to develop. A delayed increase in the responsiveness of the glands was also seen with continuous incubation of anterior pituitaries with LH-RH. The relevance of these observations to the physiological control of LH secretion is discussed.

Adrenocorticotropic Hormone↗