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At least 973 records · Page 54Linked to original sources
PubMed1994

The effect of luteinizing hormone-releasing hormone analog for central precocious puberty on growth hormone (GH) and GH-binding protein.

The pubertal growth spurt is characterized by a marked increase in the amplitude of GH secretory pulses. The high affinity GH-binding protein (GHBP) reportedly has an important role in enhancing the growth-promoting action of GH. Levels of GHBP are characteristic for an individual and increase only slightly as puberty progresses. It has been hypothesized that each individual adjusts GH production to a level appropriate for his GHBP environment. The withdrawal of gonadal steroids that occurs in children with central precocious puberty (CPP) treated with LH-releasing hormone agonist (LHRHa) therapy results in a decrease in growth velocity (GV) and GH secretion. This study was performed to determine the effect of treatment of CPP with the LHRHa leuprolide acetate for depot suspension on GH secretion and levels of GHBP. Six girls and one boy with CPP were studied before and 6 months after treatment was initiated. Within 6 months of initiation of therapy, there was a significant decline in GV, from 8.9 +/- 3.2 to 5.4 +/- 2.0 cm/yr (P < 0.05). Twelve-hour mean nocturnal GH levels decreased significantly from 8.6 +/- 3.5 to 5.1 +/- 2.3 micrograms/L (P < 0.05). This occurred via a decrease in the amplitude of GH pulses as the number of peaks remained 4.6 and 4.1/12 h. Individual levels of GHBP were variable and reflect the wide range of levels observed in normal children. Although GV and GH levels decreased substantially, mean GHBP levels remained unchanged at 139.9 +/- 46.0 and 152 +/- 39.8 pmol/L. In children with CPP, within 6 months of LHRHa therapy, the decrease in GV occurs via a decrease in nocturnal GH secretion as levels of GHBP remain unchanged. In children with CPP, the withdrawal of gonadal steroids may inhibit the child's ability to secrete the GH appropriate for his/her GH/GHBP milieu.

Body Mass Index↗
PubMed1997

Effects of luteinizing hormone-releasing hormone analog-induced pubertal delay in growth hormone (GH)-deficient children treated with GH: preliminary results.

To study the effect of delaying epiphyseal fusion on the growth of GH-deficient children, we studied 14 pubertal, treatment naive, GH-deficient patients (6 girls and 8 boys) in a prospective, randomized, placebo-controlled trial. Chronological age was 14.5 +/- 0.5 yr, and bone age was 11.6 +/- 0.3 yr (mean +/- SEM) at the beginning of the study. Patients were assigned randomly to receive GH and LH-releasing hormone (LHRH) analog (n = 8) or GH and placebo (n = 6) during 3 yr, with planned continuation of GH treatment until epiphyseal fusion. Patients were measured with a stadiometer and had serum LHRH tests, serum testosterone (boys), serum estradiol (girls), and bone age performed every 6 months. Patients treated with GH and LHRH analog showed a clear suppression of their pituitary-gonadal axis and a marked delay in bone age progression. We observed a greater gain in height prediction in these patients than in the patients treated with GH and placebo after 3 yr of treatment (mean +/- SEM, 14.0 +/- 1.6 vs. 8.0 +/- 2.4 cm; P < 0.05). These preliminary findings suggest that delaying epiphyseal fusion with LHRH analog in pubertal GH-deficient children treated with GH increases height prediction and may increase final height compared to treatment with GH alone.

Adolescent↗
PubMed1999

Reactivation of pituitary hormone release and metabolic improvement by infusion of growth hormone-releasing peptide and thyrotropin-releasing hormone in patients with protracted critical illness.

Protracted critical illness is marked by protein wasting resistant to feeding, by accumulation of fat stores, and by suppressed pulsatile release of GH and TSH. We previously showed that the latter can be reactivated by brief infusion of GH-releasing peptide (GHRP-2) and TRH. Here, we studied combined GHRP-2 and TRH infusion for 5 days, which allowed a limited evaluation of the metabolic effectiveness of this novel trophic endocrine strategy. Fourteen patients (mean +/- SD age, 68 +/- 11 yr), critically ill for 40 +/- 28 days, were compared to a matched group of community-living control subjects at baseline and subsequently received 5 days of placebo and 5 days of GHRP-2 plus TRH (1 + 1 microg/kg x h) infusion in random order. At baseline, impaired anabolism, as indicated by biochemical markers (osteocalcin and leptin), was linked to hyposomatotropism [reduced pulsatile GH secretion, as determined by deconvolution analysis, and low GH-dependent insulin-like growth factor and binding protein (IGFBP) levels]. Biochemical markers of accelerated catabolism (increased protein degradation and bone resorption) were related to tertiary hypothyroidism and the serum concentration of IGFBP-1, but not to hyposomatotropism. Metabolic markers were independent of elevated serum cortisol. After 5 days of GHRP-2 plus TRH infusion, osteocalcin concentrations increased 19% vs. -6% with placebo, and leptin had rose 32% vs. -15% with placebo. These anabolic effects were linked to increased IGF-I and GH-dependent IGFBP, which reached near-normal levels from day 2 onward. In addition, protein degradation was reduced, as indicated by a drop in the urea/creatinine ratio, an effect that was related to the correction of tertiary hypothyroidism, with near-normal thyroid hormone levels reached and maintained from day 2 onward. Concomitantly, a spontaneous tendency of IGFBP-1 to rise and of insulin to decrease was reversed. Cortisol concentrations were not detectably altered. In conclusion, 5-day infusion of GHRP-2 plus TRH in protracted critical illness reactivates blunted GH and TSH secretion, with preserved pulsatility, peripheral responsiveness, and feedback inhibition and without affecting serum cortisol, and induces a shift toward anabolic metabolism. This provides the first evidence of the metabolic effectiveness of short term GHRP-2 plus TRH agonism in this particular wasting condition.

Adult↗
PubMed2000

Near final height in pubertal growth hormone (GH)-deficient patients treated with GH alone or in combination with luteinizing hormone-releasing hormone analog: results of a prospective, randomized trial.

To study the effects of delaying puberty in GH-deficient (GHD) children, we studied 21 GHD (9 boys, 14 girls), treatment-naive, pubertal patients in a prospective, randomized trial. Their chronological age was 14.3 +/- 1.6 yr, and their bone age was 11.3 +/- 1.1 yr (mean +/- SD) at the beginning of the study. Four patients who developed hypogonadotropic hypogonadism were subsequently excluded from the study. Patients were randomly assigned to receive GH + LH-releasing hormone analog (LHRH-A) (n = 7), or GH alone (n = 10). GH and LHRH-A treatment started simultaneously in each patient. GH (Nutropin) was administered at a dose of 0.1 U/kg x day sc, until patients reached a bone age (BA) of 14 yr in girls and 16 yr in boys, and LHRH-A (Lupron depot) was administered at a dose of 300 microg/ kg every 28 days in during 3 yr. We defined GH deficiency as patients with a growth velocity less than 4 cm/yr, BA delay more than 1 yr in relationship to chronological age, GH response to two stimulation tests less than 7 microg/L, associated with low serum insulin-like growth factor I and insulin-like growth factor binding protein 3 levels. Statistical analysis was performed by ANOVA or Kruskall Wallis when variances were not homogeneous. We observed a significant decrease in the rate of BA maturation in the group treated with GH+LHRH-A (1.5 +/- 0.2 yr) compared with the group treated with GH alone (4.2 +/-0.5 yr) during the 3 years of LHRH-A therapy (P < 0.05). This delay in BA maturation produced a significant gain in final height in the group treated with GH+LHRH-A, which reached - 1.3 +/- 0.5 SD score compared with -2.7 +/- 0.3 SD score (P < 0.05) in the group treated with GH alone. These results indicate that delaying puberty with LHRH-A in GHD children during treatment with GH increases final height.

Adolescent↗
PubMed1996

Site-directed mutagenesis of recombinant equine chorionic gonadotropin/luteinizing hormone: differential role of oligosaccharides in luteinizing hormone- and follicle-stimulating hormone-like activities.

Equine chorionic gonadotropin (eCG) consists of highly glycosylated alpha- and beta-subunits and belongs to the glycoprotein hormone family that includes LH and FSH. eCG is a unique member of the gonadotropin family because it elicits response characteristics of both FSH and LH in other species than the horse. To determine the biological role of the N-linked oligosaccharide at Asn 56 of the alpha-subunit and O-linked oligosaccharides at the carboxyl-terminal peptide (CTP) of the beta-subunit, two mutant eCGs, in which Asn 56 of the alpha-subunit was replaced with Gln (eCG alpha 56/beta) or CTP was deleted (eCG alpha/ beta-CTP), were produced by site-directed mutagenesis and transfecting chinese hamster ovary (CHO-K1) cells. LH- and FSH-like activities were assayed in terms of testosterone production and aromatase activity in primary cultured rat Leydig cells and granulosa cells, respectively. The wild type eCG showed similar LH- and FSH-like activities to native eCG in the in vitro bioassays. The LH-like activity of eCG alpha 56/beta was greatly reduced, whereas that of eCG alpha/beta-CTP was unaffected, demonstrating that the oligosaccharide at Asn 56 of the alpha-subunit of eCG plays an indispensable role in LH-like activity. Interestingly, the FSH-like activity of eCG alpha 56/beta was increased markedly in comparison with the wild type, and that of eCG alpha/beta-CTP was also considerably increased. These data indicate that the dual activities of eCG, LH- and FSH-like activities, could be separated by removal of the N-linked oligosaccharide on the alpha-subunit Asn 56 or CTP-associated O-linked oligosaccharides.

Animals↗
PubMed2000

Aberrant luteinizing hormone-releasing hormone-stimulated adrenocorticotropic hormone secretion in a patient with pituitary hyperplasia due to primary hypothyroidism.

We report a patient with primary hypothyroidism associated with an aberrant ACTH response to the LH-RH test. A 40-year-old woman was admitted to our hospital displaying headache, nausea, and numbness on the left side of her face, upper limbs, and tips of her toes. Computed tomography and magnetic resonance imaging revealed a mass-like lesion in the pituitary. A high serum TSH concentration with concomitant low thyroid hormone concentrations resulted in a diagnosis of primary hypothyroidism. To exclude the possibility of a coexisting pituitary tumor including a TSH-secreting tumor, we performed dynamic TSH secretion tests. TRH testing showed an excessive, delayed TSH response, typical of primary hypothyroidism. Serum TSH decreased not only after administration of CRH, octreotide, or L-DOPA, but also after administration of LH-RH. In this case, LH-RH testing induced ACTH secretion. To determine if aberrant ACTH secretion in response to LH-RH loading is a common phenomenon in severe primary hypothyroidism, we performed the LH-RH test on 4 additional patients with pituitary enlargement due to primary hypothyroidism. Two patients demonstrated aberrant ACTH secretion in response to LH-RH loading, but the others did not. To our knowledge, this is the first report of aberrant LH-RH-stimulated ACTH secretion in primary hypothyroidism.

Adrenocorticotropic Hormone↗
PubMed1981

Dependence on protein synthesis of the N6-monobutyryl cyclic AMP plus theophylline mediated release of luteinizing hormone induced by luteinizing hormone releasing hormone from rat pituitary glands in vitro.

The involvement of cyclic AMP in the action of LH releasing hormone (LH-RH) on LH secretion was studied by incubating pituitary glands from adult female rats on day 2 of dioestrus with 1 mN-N6-monobutyryl cyclic AMP (mbcAMP) and 10 mM-theophylline for periods of up to 10 h. This treatment induced a pattern of LH release similar to that observed in the presence of a low concentration of LH-RH (0.1 ng LH-RH/ml), i.e. an initial 4 h period during which the release of LH was minimal was followed subsequently by an increased rate of release. In this system inhibition of protein synthesis by cycloheximide (25 microgram/ml) did not impair the initial response of the pituitary tissue but the increase in the rate of LH release during the second phase of the response was blocked. Preincubation with mbcAMP and theophylline increased the responsiveness of the pituitary tissue to LH-RH. This action could be prevented by including cycloheximide during the preincubation period, whereas addition of this drug during the incubation with LH-RH no longer impaired the increased responsiveness. The size of the sensitizing action of mbcAMP and theophylline mediated through the induction of protein synthesis was comparable with that of a high concentration of LH-RH. From the absence of a significant change in total LH during the preincubation period, it was concluded that the increased responsiveness was not the result of newly synthesized LH. The present results suggest a role or roles for cyclic AMP in the secretion of LH induced by LH-RH. Besides an effect on the formation of a factor related to the synthesis of protein, other than LH which has a permissive role in the acute release of LH, cyclic AMP might also be concerned in the secretion process through a pathway which does not involve synthesis of protein.

Animals↗
PubMed1982

Luteinizing hormone responses to repeated injections of luteinizing hormone releasing hormone in the rat during the oestrous cycle and after ovariectomy with or without oestrogen treatment.

In order to characterize the nature of the LH response to exogenous LH releasing hormone (LH-RH) in female rats during the oestrous cycle and after ovariectomy with or without oestrogen treatment, serum LH levels were determined after repeated LH-RH injections (300 ng/kg body wt, six times with 30-min intervals). The LH response to the first LH-RH stimulation was greatest on the days of pro-oestrus and oestrus followed by dioestrus 2 and dioestrus 1. Second and subsequent LH-RH challenges enhanced the LH response only on pro-oestrus and dioestrus 2. Larger doses of LH-RH (3 microgram/kg body wt) induced a small self-priming effect on dioestrus 1 and oestrus. The LH response to the first LH-RH administration increased with time up to 30 days after ovariectomy and then reached a plateau. A small self-priming effect was present in rats ovariectomized for 30 and 60 days, but absent in rats ovariectomized for 5, 10 and 120 days. Oestrogen treatment increased the self-priming effect in rats ovariectomized for 5 days, with little sensitization of the pituitary gland to the first LH-RH injection on the next day. In rats ovariectomized for 120 days, oestrogen treatment enhanced responsiveness to the first and successive LH-RH stimulations on the next day, and further enhancement to the first response only was induced 3 days after oestrogen treatment.

Animals↗
PubMed1983

Prostaglandin D2 induces release of luteinizing hormone from the rat pituitary gland without the modulation of hypothalamic luteinizing hormone releasing hormone.

The effect of prostaglandin D2 (PGD2) on release of LH and LH releasing hormone (LHRH) was studied in a sequential double-chamber superfusion system using the medial basal hypothalamus (MBH) and the pituitary gland from female rats at dioestrus. Infusion of PGD2 (5.7 or 57 mumol/l) caused a significant (P less than 0.05) increase in LH release to values 40-60% above the preinjection values from the pituitary gland superfused either alone or in series with the MBH. No release of LHRH in response to PGD2 was observed from the superfused MBH. These data demonstrate that PGD2 causes LH release from the pituitary gland not by inducing release of hypothalamic LHRH but by a direct action on the gland.

Animals↗
PubMed1983

Variations in hypothalamic luteinizing hormone releasing hormone content and release in vitro and plasma concentrations of luteinizing hormone and testosterone in developing cockerels.

An in-vitro superfusion system was used to study age-dependent changes in the functional activity of LH releasing hormone (LHRH) neurones terminating in the mediobasal hypothalamus (MBH) of the cockerel. Fragments of MBH tissue were obtained from cockerels killed at 8, 12, 16 and 20 weeks of age and both the rate of release of LHRH in vitro and the residual content of LHRH were determined by radioimmunoassay. Blood was collected from a similar group of cockerels of the same age for determination of plasma LH and testosterone concentrations. Superfused cockerel MBH showed both basal and depolarization-induced release of LHRH and the calcium-dependency of the release process was demonstrated. The viability of MBH in vitro was indicated by the observation that the rate of CO2 production by the tissue remained constant during a 3-h period of superfusion. Both the basal rate of release of LHRH (7.24 +/- 0.63 pg/2MBH per h; mean +/- S.E.M., n = 4) and the residual content of LHRH (1.10 +/- 0.24 ng/2MBH) were lowest in the 8-week-old cockerel and increased progressively to reach levels three (P less than 0.001) and 13 (P less than 0.001) times greater, respectively, by 20 weeks of age. Concentrations of LH and testosterone in plasma did not increase significantly until 16 weeks of age when the respective values were 5.86 +/- 0.37 micrograms/l and 1.88 +/- 0.31 nmol/l (n = 11). Whereas plasma testosterone increased further to 5.76 +/- 0.42 nmol/l (n equal 11) at 20 weeks of age, plasma LH fell significantly (P less than 0.02) to a concentration of 4.08 +/- 0.41 micrograms/l (n = 11).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1976

Effect of melatonin on the luteinizing hormone release induced by clomiphene and luteinizing hormone-releasing hormone.

The effect of melatonin on the LH-release response after the administration of synthetic LH-RH and clomiphene citrate was investigated in adult male rats. The sc administration of melatonin (1 mg/day) for 6 days produced a significant decrease in serum LH levels and in seminal vesicles and ventral prostate weights. On the other hand, the daily injection of 0.01 mg/100 g of body weight of clomiphene citrate during 6 days significantly stimulated LH levels and the weights of the accessory sex glands. Simultaneous treatment with melatonin and clomiphene produced an inhibitory effect similar to that obtained with melatonin alone. Neither pretreatment with melatonin alone. Neither pretreatment with melatonin (1 mg/day, sc for 6 days) nor its simultaneous iv administration (500 mug) with 75 ng of LH-RH modified the LH-release in response to the hypothalamic hormone. The fact that melatonin was able to suppress the effect of clomiphene, which is probably exerted at the hypothalamic level, but not the actiion of LH-RH on the pituitary, appears to indicate that the hypothalamus may be the site involved in the inhibitory effect of the pineal principle on the reproductive function.

Animals↗
PubMed2005

Final height and growth hormone secretion after completion of growth hormone therapy in patients with idiopathic growth hormone deficiency and with abnormalities of the hypothalamic-pituitary region.

AIMS: The aim of the study was an evaluation of final height and growth hormone (GH) secretion after completion of GH therapy (retesting) in patients with GH deficiency (GHD). PATIENTS AND METHODS: The analysis comprised 53 patients (43 boys, 10 girls) with childhood-onset GHD, who completed GH therapy and reached final height. Magnetic resonance imaging (MRI), performed in all the patients, led to the following groups: pituitary stalk interruption syndrome (PSIS), pituitary hypoplasia (HP), craniopharyngioma (CP) -- patients after tumour excision, patients with normal hypothalamic-pituitary region (NP). RESULTS: In 51 patients, final height was normal. The height gain was significantly (p<0.05) greater in PSIS than in that other groups. In retesting, GH secretion was significantly (p<0.005) lower in PSIS and CP than in HP and in NP and also (p<0.05) in HP than in NP. Permanent severe GHD was confirmed in all the patients with PSIS and CP and in some patients with HP (37.5%), while it was excluded in all the patients with normal pituitary in MRI. CONCLUSIONS: It seems that in patients with PSIS and CP, the confirmation of persistent character of GHD needs no retesting, while in patients with normal MRI results, GHD diagnosis should be established with special attention.

Adolescent↗
PubMed1995

Cholinergic modulation of growth hormone, prolactin and thyroid stimulating hormone responses to thyrotropin-releasing hormone in normal aging.

Endocrine changes occur during the normal aging process. These include alterations in GH, TSH and, to a lesser extent, PRL secretion. Pyrodistigmine (PD) increases basal GH secretion in a widely variable manner and partially reverses the blunted GH response to GHRH found in elderly subjects. The aims of this study were to verify the finding of a paradoxical GH response to TRH (200 micrograms iv) and to evaluate the effect of priming with PD (120 mg orally) on basal and TRH-stimulated GH, TSH and PRL secretion in 7 euthyroid subjects (aged 75-96 years). Hormonal responses after control saline and PD were also evaluated. PD did not modify TSH or PRL responses to TRH. A slight increase in GH secretion was observed after PD. A clear-cut increase in GH levels after TRH was found in 4 out of 7 subjects. TRH-induced GH secretion was significantly increased by pretreatment with PD. Functional abnormalities in the neuroendocrine control of GH secretion in aging could explain, at least in part, the appearance of GH release after TRH. Cholinergic neurotransmission, which is thought to be stimulated by PD administration, seems to be involved in the non-specific GH release after TRH administration in elderly subjects.

Age Factors↗
PubMed1976

Stimulation of growth hormone release by luteinizing hormone-releasing hormone in two males with isolated gonadotropin deficiency.

The pituitary functions were tested in two males with the typical clinical pictures of hypogonadism. The secretions of ACTH, TSH, GH and prolactin in these patients were maintained within normal limits, whereas they had markedly diminished LH and FSH levels in plasma. Plasma LH and FSH responses to the intravenous injection of 100 mug LH-RH were absent or limited. After 7-day treatment with intravenous infusion of 400 mug LH-RH, they showed normal or improved responses to the intravenous injection of 100 mug LH-RH. Thus, the diagnosis of isolated gonadotropin deficiency due to a hypothalamic lesion was established. Initially, the standard LH-RH test (100 mug intravenous injection) did not elicit a rise in plasma GH levels. However, it was of interest that after the repeated stimulation by 400 mug LH-RH, GH response to the intravenous injection of 100 mug LH-RH was observed in both patients.

Adult↗
PubMed1995

The influence of chronic administration of the serotonin agonist dexfenfluramine on responsiveness to corticotropin releasing hormone and growth hormone-releasing hormone in moderately obese people.

Evidence exists that the serotoninergic system influences the hypothalamo-pituitary-adrenal axis and pituitary GH secretion. The effect was investigated of chronic (9 weeks) administration of the serotonin receptor agonist dexfenfluramine (DF) (15 mg twice daily) versus placebo on both systems in 24 moderately obese patients with an overconsumption of snacks. Before as well as after treatment, 100 micrograms GHRH and 100 micrograms CRH was administered iv. Weight loss after 9 weeks was 3.1 +/- 2.3 kg in the DF group and 0.1 +/- 1.2 in the placebo group (p < 0.001). No significant difference between the changes in the apparently normal ACTH and cortisol response in both groups was found. The apparently low GH response did not increase or normalize, but on the contrary decreased further after DF. No changes were shown in urinary free cortisol excretion and serum IGF-I levels. It can be concluded that in moderately obese patients the use of DF during a 9-week period induced a significant weight loss, did not influence the responsiveness of the pituitary gland to CRH nor the overall activity of the pituitary adrenal axis and finally, did not normalize the blunted GH response after GHRH.

Adolescent↗
PubMed1997

Growth hormone-releasing hormone (GHRH)-GH-somatic growth and luteinizing hormone (LH)RH-LH-ovarian axes in adult female transgenic mice expressing human GH gene.

We have examined alterations in the hypothalamo-pituitary GH-somatic growth axis and the hypothalamo-pituitary LH-ovarian axis in a line of transgenic ICR mice expressing human GH (hGH) under the influence of the whey acid protein promoter. Transgenic female mice weighed twice as much as control females and were infertile. The size of the anterior pituitary (AP) was 1/3 that of the controls. In transgenic mice, acinar cells in the mammary and mandibular glands displayed hGH-immunoreactivity, and plasma hGH was detected by radioimmunoassay. In the medial basal hypothalamus (MBH) of transgenic females, the immunoreactive-GHRH level was decreased (P<0.01). There was a corresponding reduction in the number of GHRH-immunoreactive neurons in the arcuate nucleus (ARC) and in the immunostaining of GHRH nerve terminals in the median eminence. The level of somatostatin (SRIH) in the MBH was increased (P<0.05), and SRIH-immunoreactive neurons in the periventricular nucleus (PeV) were increased in size and number in transgenic mice. The MBH level of LHRH in transgenic animals was greater (P<0.01) than in controls, although there was no apparent difference in the number of LHRH-immunoreactive neurons or in LHRH level in the preoptic area. There are fewer SRIH- and LHRH-immunoreactive neurons in the ARC in transgenic mice. Cells in the AP for GH, PRL, and LH were fewer in transgenic mice. The ovary suffered disturbance of follicular development and of corpora lutea formation. These results demonstrate that chronic overproduction of hGH may profoundly affect the organization of the GHRH/SRIH-GH-somatic growth axis and the LHRH-LH-ovarian axis due to reduction of GHRH-, SRIH- and LHRH-neurons in the ARC and increase of SRIH-neurons in the PeV.

Animals↗
PubMed1984

Effect of metergoline on prolactin, follicle stimulating hormone, luteinizing hormone and thyroid stimulating hormone response to TRH and LHRH in normal men and women.

Metergoline, a prolactin (PRL)-lowering drug with an antiserotoninergic activity, is known to restore menstruations and fertility in hyper-PRL patients even when PRL levels are not normalized. This suggests that metergoline might also affect gonadotropins release. In a double-blind cross-over study in 8 normal males, repeated administration of metergoline enhanced the LH response to LHRH and reduced the PRL response to TRH; for females, three different tests were performed on days 5, 8 and 21 of two different menstrual cycles, each test being preceded by metergoline or by placebo administration. Metergoline always reduced the PRL response to TRH; on the 5th day, metergoline reduced the FSH response to LHRH and on the 21st day enhanced the LH response to LHRH. Basal levels of LH, FSH, T3, T4, Testosterone, 17 beta-estradiol and progesterone as well as the FSH response to LHRH (in males) and the TSH response to TRH (in both males and females) were not modified by metergoline. The data suggest that tests with TRH and LHRH can yield different results when performed during metergoline administration and that metergoline, acting through an unknown mechanism, can modify gonadotropins release.

Adult↗