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At least 199 records · Page 11Linked to original sources
PubMed1984

The role of endogenous opiates in the mechanism of inhibited luteinizing hormone (LH) secretion in women with anorexia nervosa: the effect of naloxone on LH, follicle-stimulating hormone, prolactin, and beta-endorphin secretion.

The aim of this study was to evaluate the role of endogenous opiates in the mechanism of decreased LH secretion in women with anorexia nervosa. For this purpose the effect of opiate receptor blockade with naloxone on LH, FSH, PRL, and beta-endorphins secretion was studied in 24 women with anorexia nervosa and 7 normal women. Serum LH, FSH, PRL, beta-endorphin-like substance, ACTH, and cortisol concentrations were measured before and after opiate receptor blockade after a single iv dose of 0.2 mg/kg naloxone or saline. Mean serum LH and FSH concentrations increased significantly after naloxone in the normal women. Eleven patients had a significant increase in serum LH concentrations in response to naloxone and 13 did not respond to naloxone with an increase in LH concentration. In the first group the basal LH values were higher than those in the second group. In the majority of patients in the first group amenorrhea preceded the wt loss, whereas in most patients in the second group amenorrhea appeared during the phase of wt loss. Naloxone did not alter pulsatile LH secretion in 6 women. No effect of naloxone on serum FSH and PRL concentrations was found. A significant increase in beta-endorphin-like substance levels after naloxone administration occurred in patients with anorexia nervosa. However, serum ACTH and cortisol concentrations were not altered in response to naloxone. In conclusion, the increase in LH release after opiate receptor blockade by naloxone suggests that endogenous opiates may play a role in the mechanism of inhibited LH secretion at least, in the majority of those women with anorexia nervosa in whom amenorrhea preceded wt loss. The results also point to a different mechanism of ACTH and beta-endorphin secretion in patients with anorexia nervosa.

Adolescent↗
PubMed2001

Pulsatile iv infusion of recombinant human LH in leuprolide-suppressed men unmasks impoverished Leydig-cell secretory responsiveness to midphysiological LH drive in the aging male.

The present investigation tests the clinical hypothesis that Leydig-cell responsiveness to pulsatile and midphysiological LH drive is impaired in older men. To this end, we implemented a novel clinical investigative paradigm consisting of preadministration of an LH-down-regulating dose (3.75 mg) of leuprolide acetate followed, 3-4 wk later, by controlled challenge of the testis, with pulsatile iv infusions of saline vs. recombinant human (rh) LH. Based on a preliminary dose-finding experiment, we evaluated LH action in 8 young (ages, 18-25 yr) and 7 older (ages, 60-85 yr) volunteers by infusing eight consecutive 6-min squarewave pulses of saline or 50 IU rhLH iv every 2 h. Analyses were carried out 48 or 72 h apart in a prospective, randomly assigned, double-blind, within-subject cross-over design. Serum concentrations of T (RIA) and LH (immunoradiometric assay) were measured in blood sampled every 10 min concurrently. Leuprolide injection suppressed pre-LH-infusion (0800 h baseline) serum T concentrations (pooled mean +/- SEM) markedly in both age groups (P < 10(-3)); namely, to 40 +/- 20 ng/dl (young) and 12 +/- 3.1 ng/dl (older; P < 0.05 vs. young) (to convert to nM, multiply by 0.0347). Successive iv pulses of rhLH stimulated T output, over time, to an asymptotic maximum of 166 +/- 42 ng/dl in young men (P = 0.0008 vs. saline) and 57 +/- 9.8 ng/dl in older subjects (P = NS vs. saline, and P < 0.05 vs. young). Further regression analyses identified significant reductions of both the initial rate and maximum of the time-dependent incremental rise in LH-driven serum T concentrations in older men. In contrast, infused serum LH concentrations, distribution volumes, and calculated LH half-lives were comparable in the two age cohorts. We conclude that older men manifest both a delayed initial and reduced maximal serum T concentration rise compared with young men exposed to identical controlled midphysiological pulsatile LH drive.

Adolescent↗
PubMed1988

Age-related changes in the secretory pattern of FSH and LH in response to LH-RH in prepubertal female rats.

Developmental changes in the pituitary responsiveness and the secretory pattern of FSH and LH in response to a single injection of LH-RH (100 ng/rat, s.c.) as estimated by increases in plasma concentrations of FSH and LH 10, 30 and 60 min after the injection were studied in female rats at 5, 10, 15, 20, 25 and 30 days of age. The pituitary responsiveness to LH-RH for both FSH and LH release increased from 5 to 15 days of age, reached a maximum on 15 days of age and declined thereafter, whereas a marked increase in the amount of these hormones in the pituitary occurred between 15 and 20 days of age. An apparent change in the secretory pattern of both FSH and LH was observed from 20 days of age onward. In groups up to 15 days of age, plasma concentrations of FSH and LH remained elevated 60 min after the injection of LH-RH, though the plasma concentration of these hormones returned to preinjection concentrations in groups at 20 days of age or later. These results indicate that the age-related changes in the secretory pattern of LH and FSH in response to LH-RH as well as changes in the pituitary responsiveness were apparent during the prepubertal period.

Age Factors↗
PubMed2001

In vitro effect of leptin on LH release by anterior pituitary glands from female rats at the time of spontaneous and steroid-induced LH surge.

OBJECTIVE: The purpose of this work was to study the direct effect of leptin on LH release by anterior pituitary glands from female rats at the time of spontaneous and steroid-induced LH surge. METHODS: LH responsiveness to leptin by pituitaries from rats killed in the afternoon (1500 h) at different stages of the 4-day estrous cycle (diestrus-1: D1; diestrus-2: D2; proestrus; estrus), ovariectomized (OVX; 15 days post-castration) and ovariectomized steroid-primed (OVX-E(2)/Pg; pretreated with 5 microg estradiol and 1 mg progesterone), was evaluated in vitro. Hemi-adenohypophyses were incubated in the presence of synthetic murine leptin for 3 h. RESULTS: Addition of increasing concentrations of leptin (0.1-100 nmol/l) to the incubation medium of proestrus pituitaries produced a dose-related stimulation of LH release; the maximal increase to 315% of control was obtained with 10 nmol/l leptin. Leptin (10 nmol/l) enhanced LH release at all days of the estrous cycle, the greatest response occurring in proestrus (318%) and the lowest at D1 (123%). In order to evaluate the role of nitric oxide (NO) in the action of leptin on LH release, glands from proestrus rats were incubated in the presence of 10 nmol/l leptin with or without 0.3 mmol/l N(G)-monomethyl-l-arginine (NMMA), a competitive inhibitor of NO synthase (NOS). NMMA completely suppressed the stimulation of LH release induced by leptin. Leptin also stimulated LH release by pituitaries from OVX rats, and treatment with steroid hormones led to a marked increase in the response (OVX: 162% compared with OVX-E(2)/Pg: 263%; P<0.05). For comparative analysis, a similar experimental procedure was carried out using GnRH (10 nmol/l). Leptin acts at the pituitary level in a similar manner as GnRH, although with significantly lower potency. CONCLUSIONS: These results confirm and extend previous reports regarding a direct action of leptin at the pituitary level, stimulating LH release by anterior pituitaries from female rats at the time of spontaneous and steroid-induced LH surge. In the female rat pituitary this leptin action is controlled by gonadal steroids and mediated by NO.

Animals↗
PubMed1987

Role of LH pulse amplitude and the rate of LH increase on oestradiol-17 beta secretion by immature rat ovaries in perfusion culture.

Immature rat ovaries were placed in perifusion culture and exposed to LH in a variety of patterns, while tonic levels of FSH (200 ng/ml) were maintained. Perifusate was collected every 5 min and assayed for oestradiol-17 beta. In Exp. I, LH was delivered at 50 ng/ml for 30 min then reduced to 0 ng/ml for an additional 30 min (50 ng/ml LH step) or as linear increasing concentrations reaching 50 ng/ml by 30 min of culture then linear decreasing concentrations reaching 0 ng/ml by 30 min of culture (50 ng/ml LH ramp). Although both delivery systems exposed the tissue to 250 ng LH over the 1-h culture period, only the 50 ng/ml step significantly increased oestradiol-17 beta secretion rates (P less than 0.05). In Exp. II, ovaries were not exposed to LH for the first 30 min of culture but then LH was administered at a concentration of 25 or 50 ng/ml for 30 min. The LH concentration was reduced to 0 ng/ml for an additional 30 min of culture. Oestradiol-17 beta secretion rates were increased 50% by both treatments. These results suggest that the mechanism by which an LH pulse stimulates the immature ovary to secrete oestradiol-17 beta is, in part (1) 'threshold'-dependent and not solely dependent on the amount of LH administered, and (2) dependent on the time required to achieve a 'threshold' level.

Animals↗
PubMed1993

Maturational changes in gonadotrophin secretion: the LH response to realimentation and a nocturnal increment in LH secretion of feed-restricted prepubertal gilts.

Potential maturational changes in patterns of LH secretion during feed restriction and the LH response to realimentation were examined. Ten sets of four growth-matched littermate gilts were fed ad libitum, to reach either 55, 65, 75 or 85 kg target body weights (one littermate per weight). Gilts were then maintenance fed for 8 days (days 1-8), and to appetite on day 9, and kept in a 9 h light (07:00-16:00 h):15 h dark photoperiod. Blood samples were obtained every 10 min from 07:00 to 16:00 h, and from 16:00 to 24:00 h on day 8 to evaluate any nocturnal rise in LH, and from 07:00 to 16:00 h on day 9 to evaluate the LH response to realimentation. Radioimmunoassays for LH, FSH, melatonin and oestradiol were performed on selected plasma samples. In all three sampling periods, LH and FSH secretion decreased as gilt weight increased, in a quadratic manner. During feed restriction, daytime LH, but not FSH, secretion was lower than at nighttime, irrespective of weight. Daytime LH secretion increased in response to realimentation, irrespective of weight. Plasma oestradiol concentrations were increased by feed restriction and decreased by realimentation but showed little relationship to gilt weight. No consistent relationship was established between plasma melatonin concentrations and ambient illumination. In conclusion, LH secretion exhibits a diurnal rhythm during feed restriction in the prepubertal gilt and, in a similar way to FSH, decreases as puberty is approached. The plane of nutrition influences circulating oestrogen concentrations. The increase of LH secretion following realimentation is not influenced by maturation over the prepubertal period.

Animals↗
PubMed2001

The fourth International Standard for Human Urinary FSH and LH: specificities of LH seminal vesicle weight gain assays in the collaborative study differ between laboratories.

The fourth International Standard for Human Urinary FSH and LH (IS; in ampoules coded 98/704) was compared with the third International Standard for Urinary FSH and LH (IS 71/264) by 10 laboratories in nine countries, using FSH and LH in vivo bioassays. Estimates of the FSH content of the IS by augmented ovarian weight gain assays were homogeneous within each laboratory and over all laboratories. The combined weighted geometric mean estimate of FSH content of the IS (with 95% fiducial limits) in terms of IS 71/264 was 71.9 (69.0-74.9) IU/ampoule. Although estimates by seminal vesicle weight gain (SVW) assays of the relative LH activities of the IS and IS 71/264 were homogeneous within laboratories, estimates were heterogeneous between laboratories. This indicated differences between the spectrum of LH isoforms in the IS and IS 71/264, which were obtained from different manufacturers, and differences between the specificities of SVW assays performed in different laboratories. The differences between the specificities of SVW assays appeared to be related to interactions among mean laboratory seminal vesicle weights, age and genetic strain of rat. The finding of inter-laboratory differences in the specificities of SVW assays is of some significance, as this assay method has been generally adopted by Pharmacopoeias for the control of the LH content of therapeutic products. The combined unweighted geometric mean estimate of LH content of the IS (with 95% fiducial limits) in terms of IS 71/264 by SVW and ovarian ascorbate depletion assays was 70.2 (61.7-80.0) IU/ampoule. Estimates of the FSH and LH content of ampoules of the IS kept at increased temperatures suggested that the IS would be adequately stable under normal storage conditions. On the basis of these results, the World Health Organization Expert Committee on Biological Standardization established the preparation in ampoules coded 98/704 as the fourth International Standard for Human Urinary FSH and LH, and assigned to the contents of each ampoule an activity of 72 International Units of urinary FSH and an activity of 70 International Units of urinary LH.

Animals↗
PubMed1975

Rhythmic patterns of endogenous LH release in castrate sheep receiving exogenous LH (38477).

Exogenous ovine LH was constantly infused during 6-hr experimental sequences in order to determine the effect of elevated levels of plasma LH on the pulsatile discharges of pituitary LH characteristic of ovariectomized sheep. Plasma LH concentrations (exogenous plusendogenous) in sequential 10-min samples continued to fluctuate significantly as did plasma LH (endogenous only) during control periods. The temporal patterns of plasma LH during LH infusion were at least as as rhythmic as they were in the controls. Furthermore, the mean periods for extremely rhythmic frequencies were equivalent in control and LH-infusion sequences. These data refute the original hypothesis that inhibitory short-looped feedback of circulating LH governs the timing of subsequent LH discharges in ovariectomized sheep.

Animals↗
PubMed1994

Effect of adenylate cyclase inhibitor and protein kinase C inhibitor on GnRH-induced LH release and LH beta subunit biosynthesis in rat anterior pituitary cells.

According to our previous studies together with others, GnRH, a hypothalamic decapeptide, has been known to be a major regulator for LH release and its subunit biosynthesis in anterior pituitary gonadotropes. But the precise mechanisms by which GnRH exerts stimulatory effects on LH release and its subunit biosynthesis have not been clearly understood. In the present study we examined the effect of GnRH on protein kinase C (PKC) activity and intracellular cAMP content in cultured anterior pituitary cells of rat to clarify whether PKC or cAMP are involved in GnRH action. Moreover, we examined the effects of staurosporine (ST), a PKC inhibitor and 2',3'-dideoxyadenosine (2',3'-DDA), an adenylate cyclase inhibitor, on LH release and steady state LH beta subunit mRNA levels in cultured anterior pituitary cells of rat. PKC activity was rapidly increased within 30 min after GnRH treatment whereas intracellular cAMP level was elevated 18 h after GnRH treatment. ST significantly inhibited GnRH-induced LH release and LH beta subunit mRNA levels in a dose-dependent manner, showing an half maximal response at 50 nM ST. 2',3'-DDA inhibited GnRH-induced LH release and LH beta subunit mRNA levels in a dose-dependent manner in pituitary cells. From these results, it is suggested that GnRH stimulates LH beta subunit mRNA level as well as LH release in anterior pituitary cells and this GnRH action might be mediated by PKC activation and cAMP stimulation.

Adenylyl Cyclase Inhibitors↗
PubMed1975

LH and FSH response to synthetic LH-RH in children and adolescents with Turner's and Klinefelter's syndrome.

Stimulation with LH-RH (luteinizing hormone-releasing hormone) was performed in 29 children and adolescents with Turner's syndrome (15 less than 13 years old), and in 11 patients with Klinefelter's syndrome (7 before puberty). Synthetic LH-RH was injected intravenously in a dose of 25 mug/m2; plasma LH and FSH were determined radioimmunologically. The results show that patients with Turner's syndrome had pathologically elevated LH and FSH values at all ages. Normal LH and FSH results before and after LH-RH were found in 3 patients with X0/XX karyotype who had spontaneous menstruation. The 2 adult patients with Klinefelter's syndrome showed an exaggerated LH response and excessively high FSH levels before and after LH-RH, consistent with hypergonadotropic hypogonadism. Six out of 7 prepubertal boys with Klinefelter's syndrome, had a normal LH and FSH response to LH-RH. Only 1 prepubertal boy with cryptorchidism and genital maliformation in addition to the Klinefelter's syndrome had pathological values. The normal gonadotropin results in prepubertal patients with Klinefelter's syndrome show that their testes apparently loose the negative feedback activity on gonadotropin secretion only during puberty, at a time when tubular hyalinization appears. This is in contrast to Turner patients with gonadal dysgenesis who have hypergondadotropic hypogonadism already early in childhood.

Adolescent↗
PubMed1979

Changes of serum testosterone and of LH-RH test after treatment of cryptorchidism by intranasal LH-RH.

The aim of the present investigation was to study, in a collaborative double-blind study, the treatment with intranasal LH-RH application of boys aged 1 1/2 to 12 years, who suffered from unilateral or bilateral cryptorchidism. A total of 88 subjects were randomly and blindly allocated to LH-RH and placebo therapy. Before and after 4 weeks of treatment basal testosterone serum levels were estimated and LH-RH tests were performed. Intranasal treatment with LH-RH resulted in partial or complete descents of testes in 23 out of 88 patients, whereas the position of testes remained unchanged in 17 subjects. 42 boys did not respond to placebo therapy, but complete descents were observed in 6 boys of the placebo group. Hormone analysis data of 4 different laboratories were recorded and statistically evaluated. No changes of LH, FSH and testosterone were found in the placebo groups. Only patients of the Frankfurt group responded to LH-RH test with augmented LH release after therapy (P less than 0.05). All patients treated with intranasal LH-RH showed a significant decrease of FSH release after therapy (P less than 0.05 to P less than 0.01). Basal testosterone serum levels were found to be increased after therapy only in the patients treated at Zürich (P less than 0.05). Data of the present study combine to suggest that chronic application of LH-RH may result in an overstimulation phenomenon, and that LH-RH test as well as basal testosterone levels cannot be used as prognostic index of therapy efficacy.

Administration, Intranasal↗
PubMed1994

The concentration of LH-RH receptors in the nuclei of pancreatic cancer cells. Effect of (D-Trp6)LH-RH on tumor-bearing Syrian golden hamsters.

LH-RH analogs cause some inhibition of growth of pancreatic cancers. Syrian golden hamsters bearing chemically induced pancreatic cancers were treated with [D-Trp6]LH-RH for 3 d before sacrifice. LH-RH receptors were localized by electron-microscopic immunohistochemistry in the tumor cells of both treated and untreated hamsters. [D-Trp6]LH-RH treatment resulted in a marked increase in the concentration of LH-RH receptors in the nuclei. The dissociation constants (Kd) and the maximal binding capacity of the LH-RH receptors (Bmax), measured by radioreceptor assay, were higher in the nuclei of the pancreatic tumor cells of hamsters treated with [D-Trp6]LH-RH than in the untreated controls. Pancreatic cells of tumor-free hamsters did not show immunostaining for LH-RH receptors. A possible correlation between the increase in the concentration of the LH-RH receptors in the nuclei and the tumor growth-inhibiting activity of [D-Trp6]LH-RH is suggested.

Animals↗
PubMed1989

Comparison of monoclonal luteinizing hormone (LH) receptor antibody and LH binding sites in vibratome sections of rat ovary by immunohistochemistry.

To identify luteinizing hormone (LH) receptors, a monoclonal antibody (MAb) was produced by immunization of Balb/c mice with rat luteal cell membranes. Hybridomas, produced by a method for proteins of low antigenicity, were selected by competition with [125I]-hCG (LH) for luteal membrane binding. Conditions for analysis of LH receptor antibody (IgG2b isotype) binding by immunohistochemistry with an avidin-biotin-peroxidase complex were examined and results compared to localization of bound hCG, to detect receptors. By light microscopy, both bound hCG and the LH receptor antibody were located on luteal cell surfaces. In addition, the LH receptor antibody was associated with luteal cell cytoplasm. Cell surface membrane binding, but not cytoplasmic staining, was reduced in ovaries from rats injected with hCG. By electron microscopy, LH receptor antibody was observed in patches on luteal cell surface membranes and was associated with polysomes, small vesicles, and occasionally with discrete areas of endoplasmic reticulum. Therefore, detection of LH receptors with bound hCG may be limited to receptors found on cell surfaces, while additional LH receptors are revealed by use of a receptor antibody. The cytoplasmic LH receptor may represent stages in the processing of receptor protein. Furthermore, the methodology used in this study should be generally useful for immunohistochemistry with other MAb to receptors.

Animals↗
PubMed1984

Inhibition of synthesis of luteinizing hormone (LH) receptors by a down-regulating dose of LH.

Although LH is known to cause down-regulation of the LH/human CG (hCG) receptor, the mechanisms underlying this process are not well understood. Here we have analyzed the effects of LH on the turnover of LH receptors in cultured granulosa cells. Down-regulation was stimulated in FSH-primed granulosa cells by exposure to LH for 1 h. By 24 h after LH exposure, the LH/hCG receptor content, as measured using [125I]iodo-hCG was 70% less than controls. To determine whether this loss of LH/hCG receptors was due to accelerated receptor degradation, turnover measurements were made using tunicamycin to inhibit LH/hCG receptor synthesis. Under these conditions, there was a small (16%) increase in the rate of degradation of LH/hCG receptors in LH-treated cells compared to controls. By contrast, the rate of LH/hCG receptor synthesis, estimated mathematically, was reduced by 75% in the LH-treated cells. LH treatment had no effect on the incorporation of [35S]methionine into total cellular protein. Withdrawing FSH from the culture medium had a similar effect, slightly enhancing LH/hCG receptor degradation while markedly reducing its synthesis. The role of lysosomes in the degradation of LH/hCG receptors was also investigated. The lysosomotropic amine NH4Cl failed to cause LH/hCG receptors to accumulate, contrary to what would be expected if LH/hCG receptors were degraded lysosomally. In contrast, NH4Cl inhibited the degradation of receptor-bound [125I]iodo-hCG, suggesting that the ligand and the receptor may be handled differently by the granulosa cell. Our results suggest that in the granulosa cell, LH down-regulates its own receptor by inhibiting the synthesis of LH/hCG receptors, possibly by interfering with the ability of FSH to stimulate the synthesis of LH/hCG receptors. Furthermore, they suggest that the degradation of LH/hCG receptors may occur by nonlysosomal mechanisms.

Animals↗
PubMed1985

Differences in the lateral mobility of receptors for luteinizing hormone (LH) in the luteal cell plasma membrane when occupied by ovine LH versus human chorionic gonadotropin.

Receptors for LH are internalized by ovine luteal cells 50 times slower when occupied by hCG than when occupied by ovine LH (oLH). To determine if differences in the rate of internalization were due to differences in the lateral mobility of the hormone-receptor complexes in the cell membrane, the diffusion coefficients of oLH- and hCG-LH receptor complexes were measured using fluorescence photobleaching recovery methods. Tetramethylrhodamine isothiocyanate (TRITC)-labeled oLH and hCG, which retained full ability to bind to receptor, were bound to LH receptors on enzymatically dispersed ovine luteal cells. Molecules labeled with TRITC within a 3-micron 2 region of the cell surface were bleached by a 500-msec pulse of 3 mW laser light at a wavelength of 514.5 nm. The laser beam intensity was then attenuated 20,000-fold, and fluorescence from the bleached area was measured by single photon counting as unbleached fluorescent hormone-receptor complexes diffused into the region. Data were analyzed on-line by a NOVA 3/12 computer. The oLH-LH receptor complex had a diffusion coefficient of 1.9 +/- 1.0 X 10(-10) cm2/sec-1, a value comparable to that of cell surface proteins nonspecifically labeled with succinylated Concanavalin A. Fluorescence recovery after photobleaching was 35%. In contrast, hCG-LH receptor complexes were immobile on the time scale of the experiment, implying that the diffusion coefficient was substantially less than 1 X 10(-11) cm2/sec-1. Deglycosylated hCG-TRITC bound to LH receptor had a diffusion coefficient (1.1 +/- 0.1 X 10(-10) cm2/sec-1) similar to that of receptors occupied by oLH. Thus, it appears that the carbohydrate portion of the hCG molecule plays a role in decreasing the mobility of the receptor for LH. These data demonstrate that the rate of lateral movement of the LH receptor in the plasma membrane of luteal cells appears to be modulated by the nature of the bound hormone.

Animals↗
PubMed2003

Absence of exon 10 of the human luteinizing hormone (LH) receptor impairs LH, but not human chorionic gonadotropin action.

The LH receptor (LHR) mediates the actions of LH and human chorionic gonadotropin (hCG). In vivo data showed that deletion of exon 10 does not affect hCG action, whereas LH action is impaired. To investigate the role of exon 10 in LH/hCG action in vitro we created stable COS-7 cells expressing the LHR with (wt) or without (-ex10) exon 10. Binding experiments showed that the affinities of LH and hCG to the LHR wt and -ex10 were similar. Stimulation of wt with hCG or LH resulted in increased cAMP. cAMP production was significantly impaired in -ex10 stimulated with LH. This response was not altered by pertussis toxin, excluding that G(i) becomes activated in LHR -ex10. In desensitization experiments, intracellular cAMP of LHR wt and -ex10 declined to approximately 30%. No difference in intracellular cAMP was detected between LHR wt or -ex10 after recovery and restimulation with hCG or LH. These experiments show that impaired cAMP production of LHR -ex10 stimulated with LH is not due to anomalous receptor coupling or desensitization. We conclude that although exon 10 of the LHR plays no role in ligand binding, it is important for receptor activation by LH by a mechanism probably involving extracellular conformational changes.

Animals↗
PubMedDate not supplied

The pattern of LH release in the adult ram influences the testicular steroidogenic response to individual LH pulses and is regulated by testosterone negative feedback.

Two experiments were conducted with adult intact rams (approximately 58 kg in body weight) in the nonbreeding season to investigate interrelationships between LH and testosterone secretion. In Experiment 1, LH pulse frequency was increased from approximately two to six peaks per 8 hours (for 56 hours) by injecting (iv) 10 micrograms NIH-LH-S18 every 80 minutes. Induction of a breeding season peak frequency produced a progressive 3-fold increase (P less than 0.01) in mean serum testosterone levels to values during the last 8 hours of treatment (12.6 +/- 1.2 ng/ml) that were 50% of those in the fall. In response to LH pulsing, testosterone peak amplitude increased (P less than 0.05) from 3.5 +/- 0.8 ng/ml to 6.7 +/- 0.7 ng/ml. In Experiment 2, the mean testosterone level was increased to breeding season values (for 96 hours) by injecting (im) 5 mg testosterone every 4 hours. Mean LH levels and LH peak frequency were decreased (approximately 70%, P less than 0.01) following 36 hours of treatment, and the LH response to exogenous GnRH was decreased (approximately 45%, P less than 0.01) by the final 4 hours Results indicate that for rams in the nonbreeding season, the testicular steroidogenic response to individual LH pulses is enhanced when pulse frequency is increased. When blood testosterone is elevated to breeding season levels, LH pulse frequency is severely impaired, while pituitary responsiveness to GnRH is diminished, as in the fall.

Animals↗