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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The direct pituitary effects of estrogen and progesterone on the secretion of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) were studied in ovariectomized (OVX) ewes in which the pituitary had been disconnected surgically from the hypothalamus (hypothalamo-pituitary disconnection, HPD). Gonadotropin secretion was restored with hourly pulses of 500 ng gonadotropin-releasing hormone (GnRH) via intra-atrial cannulae. Intramuscular injections of 50 micrograms estradiol benzoate (EB) to 5 sheep initially caused reductions (approximately 50%) in plasma LH baseline, peak values and LH pulse amplitude. Thereafter all parameters of plasma LH concentration increased 2- to 3-fold above starting values. After these 5 sheep had received 2 subcutaneous progesterone implants (mean +/- SEM plasma levels 5.3 +/- 1.5 nmol/l), the biphasic LH response to EB was still apparent and increases in LH peak values (267 +/- 19%) and LH pulse amplitudes (262 +/- 23%) were greater (p less than 0.05) than those seen with EB alone (195 +/- 11 and 172 +/- 14%, respectively). The presence of 2 progesterone implants alone did not change plasma LH baseline, peak values or pulse amplitude, or plasma FSH values. In the second experiment, where 4 OVX-HPD ewes were given 4 progesterone implants (plasma progesterone 27.7 +/- 3.4 nmol/l), there were no effects on basal plasma LH or plasma FSH values. The LH responses to EB were more marked in 4 OVX-HPD ewes given 4 progesterone implants than in the animals given EB alone. Also, the estrogen-induced LH surge occurred earlier in the ewes given 4 progesterone implants than in those given estrogen alone.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Direct pituitary effects of estrogen and progesterone on gonadotropin secretion in the ovariectomized ewe. 643 45

To further assess quantitative pituitary gonadotropin release in patients with primary hypogonadism, a 3-hour constant infusion of the synthetic gonadotropin-releasing hormone, LH-RH, was administered to 12 functionally agonadal girls (11 with Turner syndrome and 1 who had been overiectomized), aged 9.5 to 19.42 years. Gonadotropin and sex steroid responses were determined before and during the infusion and contrasted to those in normal pubertal females. in girls with skeletal age under 11 years, mean control LH increased (P < .001) from 2.2 +/- 0.3 (mean +/- SEM) mIU/ml to 21.3 +/- 7.3 during LH-RH infusion, while luteinizing hormone (LH) rose (P < .001) from 89.2 +/- 24.6 to 276.5 +/- 42.6 girls with skeletal age over 11 years. This age-related augmentation is an exaggeration of data in normal girls and occcurs despite minimal gonadal secretion of sex steroids. A similar age-related discrepancy was not seen in follicle-stimulating hormone (FSH) secretion evoked by LH-RH; all girls had FSH increments into the castrate range with a rise from mean control levels of 78.6 +/- 6.7 to 133.9 +/- 8.3. These data demonstrate an age-related increase in LH-RH-evoked LH secretion, but not of FSH, in children and adolescents with primary hypogonadism.
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PMID:Responses to constant infusion of LH-RH in girls with primary hypogonadism. 644 63

Plasma luteinising hormone (LH) and follicle-stimulating hormone (FSH) concentrations were measured before and after intravenous luteinising hormone-releasing hormone (LH-RH) in 33 boys with growth delay. Eighteen were prepubertal and 15 pubertal. Basal LH and FSH levels were low in both groups with mean increments after LH-RH of 3.2 +/- 0.8 U/l (mean +/- SEM) and 2.6 +/- 0.4 U/l respectively in the prepubertal and 7.4 +/- 0.7 U/l and 2.0 +/- 0.3 U/l in the pubertal boys. The LH increment showed a positive correlation with increasing bone age (r = 0.71, P less than 0.001); FSH did not. The LH-RH response thus appeared normal in relation to the stage of maturity.
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PMID:Gonadotrophin response to LH-RH in boys with delayed growth and adolescence. 679 93

Concentrations of human chorionic gonadotrophin (beta-hCG), follicle-stimulating hormone (FSH), luteinizing hormone (LH) and prolactin (PRL) were measured by radioimmunoassay in the serious fluid of hydatid vesicles obtained from 27 patients with hydatidiform mole. High amounts of all four hormones were found in every case. The mean concentrations +/- SEM were 710.8 +/- 100.8 i.u./1 X 10(-3) for beta-hCG, 13.8 +/- 0.3 i.u./1 for FSH, 302.2 +/- 34.5 i.u./1 X 10(-3) for LH and 2610.8 +/- 562.1 m-i.u./1 for PRL. It is suggested that aberrations in the mechanisms controlling the synthesis and release of luteinizing hormone-releasing factor (LH-RF) could result in chronically elevated LH levels leading to changes characteristic of the disease.
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PMID:Elevated intravesicular fluid luteinizing hormone concentration in hydatidiform mole. 680 70

The responses of anesthetised fetal pigs (n=95) and chronically catheterized fetal pigs (n=10) to luteinizing hormone releasing hormone (LHRH) administration (2 micrograms/kg estimated fetal body weight) was investigated. Fetuses were studied at 55, 70, 85, 100, 106 (chronic) and 113 days. Plasma concentrations of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) were measured by radioimmunoassay. Blood samples were taken from the umbilical artery (anesthetised fetuses) or carotid artery (catheterized fetuses) every 10 min for 1 h except in the youngest age group. No significant sex difference in the LH response to LHRH treatment was observed. The LH response increased with gestational age; average pretreatment plasma concentrations were below 1.1 ng/ml. No response was observed at 55 days, and the highest response was seen at 113 days when plasma LH concentrations rose to 4.3 +/- 0.7 (mean +/- SEM) ng/ml 40 min after treatment. Pretreatment plasma FSH concentrations at 55 days were 1.6 +/- 0.1 ng/ml and gradually rose in males to 3.2 +/- 0.4 ng/ml at 113 days, which was significantly lower than in females where concentrations averaged 8.1 +/- 2.0 ng/ml. LHRH did not significantly affect FSH concentrations in males, while in females a gradually increasing response was observed; at 113 days plasma FSH was 12.5 +/- 2.9 ng/ml 40 min after treatment. The increase in response to LHRH with age of plasma LH concentrations in both sexes, and of plasma FSH concentrations in females indicates the maturation of the hypothalamo-pituitary system.
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PMID:Response of luteinizing hormone and follicle-stimulating hormone to luteinizing hormone releasing hormone in the fetal pig. 681 43

Five species of felids (cheetah, North Chinese leopard, tiger, lion, and puma) were serially injected with a source of follicle-stimulating hormone (FSH) to evaluate its effect on ovarian activity. Animals were subjected to laparoscopy before and after gonadotropin treatment, and the number and appearance of mature ovarian follicles (MF), corpora hemorrhagica (CH), and corpora lutea (CL) were recorded and photographed. Ovarian morphologic features, including MF, CH, and CL anatomy, were similar among various species. A dosage of 10 mg of FSH given IM daily for 3 to 5 days was effective in stimulating ovulation in 8 of 8 cheetahs. The same dosage for 5 days stimulated ovulation in 6 of 7 North Chinese leopards, 4 of 7 tigers, 2 lions, and 1 puma. An injection of a luteinizing hormone source was not required to induce follicular rupture. The number of ovulations eventually obtained appeared related to the activity prior to FSH treatment. Females with evidence of follicular development prior to treatment eventually produced a combined average (+/- SEM) of 5.2 +/- 1.3 CH and CL, in comparison with 2.3 +/- 0.8 CH and CL observed in cats with no identifiable follicles before FSH injection. The species varied in the number of ovulation sites (combined number of CH and CL) after treatment, with the cheetahs, leopards, tigers, lions, and puma producing a mean of 5.5 +/- 0.9, 1.5 +/- 0.2, 4.7 +/- 3.1, 1.5 +/- 0.5, and 3.0 +/- 0.0, respectively. The cheetahs, North Chinese leopards, and tigers failed to develop a refractory response to the gonadotropin, as certain females receiving FSH twice at a 1-year interval produced a similar ovulatory response.
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PMID:Gonadotropin regimen for inducing ovarian activity in captive wild felids. 681 75

Glycoprotein hormone alpha-subunit (alpha SU) is a recognized product of clinically non-functioning, glycoprotein hormone-secreting and somatotroph adenomas but has not been studied systematically in corticotroph tumours. We have performed immunohistochemistry for alpha SU in a consecutive series of four corticotroph tumours causing Nelson's syndrome, three corticotroph macroadenomas, 12 corticotroph microadenomas and one adrenocorticotrophin-secreting bronchial carcinoid tumour. In addition we have assessed alpha SU secretion in vitro in corticotroph adenomas from two subjects with Cushing's disease and two subjects with Nelson's syndrome. Immunohistochemistry, performed after microwave treatment of sections to enhance antigen retrieval, demonstrated alpha SU positivity in 3/4 Nelson's tumours, 2/3 corticotroph macroadenomas, 7/12 microadenomas and one bronchial carcinoid. Eight of the 13 tumours positive for alpha SU were also immunostained after microwave pretreatment of sections for thyrotrophin (six positive), follicle-stimulating hormone (four positive), luteinizing hormone (three positive), beta-chorionic gonadotrophin (five positive), growth hormone (three positive) and prolactin (two positive) immunoreactivity. In vitro cell cultures of all four tumours studied secreted adrenocorticotrophin and three secreted alpha SU, with the variable presence of luteinizing hormone, follicle-stimulating hormone, thyrotrophin, growth hormone and prolactin, in basal culture. The alpha SU secretion was augmented by phorbol ester (160 +/- 15%, SEM, n = 3 wells; p < 0.01) and 8-bromo-cAMP (138 +/- 8%; p < 0.05) in one tumour. These data indicate that plurihormonality and, in particular, alpha SU elaboration and secretion by corticotroph tumours is more common than hitherto recognized. Possible mechanisms include abnormal or deregulated gene expression, autocrine or paracrine effects or a stem cell origin of tumour.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Glycoprotein hormone alpha-subunit production and plurihormonality in human corticotroph tumours--an in vitro and immunohistochemical study. 754 79

The aim of the study was to elucidate the role of the neuropeptide galanin in the regulation of somatotropic and gonadotropic function in normal women. Thirteen normally ovulating (aged 28 to 40 years), non-obese (body mass index, 18.4 to 27.1 kg/m2) women with infertility due to a tubal or male factor were studied. Each woman underwent three tests: (1) bolus intravenous (IV) injection of growth hormone (GH)-releasing hormone (GHRH) (1-29)NH2 1 microgram/kg plus gonadotropin-releasing hormone (GnRH) 100 micrograms at time 0; (2) IV infusion of porcine galanin 500 micrograms in 100 mL saline from -10 minutes; and (3) bolus IV injection of GHRH(1-29)NH2 1 microgram/kg plus GnRH 100 micrograms at time 0 plus IV infusion of porcine galanin 500 micrograms in 100 mL saline from -10 to +30 minutes. All results are expressed as the mean +/- SEM. GH peak after GHRH was 14 +/- 5 micrograms/L; porcine galanin significantly increased serum GH (GH peak, 7.3 +/- 1.2) with respect to baseline levels. No significant differences were observed between either GH peak or GH absolute values after galanin as compared with GHRH alone. Porcine galanin significantly enhanced GH response to GHRH (peak, 31.4 +/- 4.4 micrograms/L) with respect to either GHRH or galanin alone. Luteinizing hormone (LH)/follicle-stimulating hormone (FSH) peaks after GnRH were 16.5 +/- 5.3 and 17.4 +/- 4 IU/L, respectively. Porcine galanin did not cause significant increases in serum LH and FSH levels with respect to baseline.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Role of galanin in the regulation of somatotrope and gonadotrope function in young ovulatory women. 754 51

It is well established that the central alpha 2-adrenergic agonist clonidine can enhance growth hormone (GH) secretion in humans. This effect is most likely due to stimulation of hypothalamic growth hormone releasing hormone (GHRH) release. To determine the potency of the new I1-imidazoline receptor agonist moxonidine to release pituitary hormones, 12 normal volunteers received clonidine (0.3 mg), moxonidine (0.3 mg), or placebo orally according to a randomized, double-blind protocol. Blood was drawn prior and up to 180 min after drug administration for determination of GH, adrenocorticotropic hormone (ACTH), prolactin, thyrotropin (TSH), luteinizing hormone (LH), follicle-stimulating hormone (FSH), glucose, clonidine, and moxonidine concentrations. The results were compared to those obtained in a standard GHRH stimulation test (1 microgram/kg i.v.). Serum GH levels increased significantly in response to GHRH, clonidine, and moxonidine. However, the increase was less pronounced in response to clonidine and moxonidine as compared to GHRH (mean +/- SEM): after clonidine, GH increased from 0.2 +/- 0.1 to 5.4 +/- 1.5 ng/ml, p < 0.05; moxonidine increased GH levels from 0.1 +/- 0.04 to 4.8 +/- 1.9 ng/ml (p < 0.05); GHRH caused an increase from 0.01 +/- 0.05 to 14.8 +/- 2.5 ng/ml (p < 0.05). No significant change was observed in the concentration of any other pituitary hormone. We conclude that the new I1-imidazoline receptor agonist moxonidine stimulates GH release to a similar extent as clonidine.
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PMID:Growth hormone secretion in response to the new centrally acting antihypertensive agent moxonidine in normal human subjects: comparison to clonidine and GHRH. 758 24

Because there is an unexpected action of testosterone (T) to increase follicle-stimulating hormone (FSH) production in the absence of gonadotropin-releasing hormone (GnRH) in the rat, the effects of T treatment on circulating FSH were studied in men with GnRH deficiency. FSH immunoreactivity was identified in serum using a sensitive two-site immunoassay in each of five untreated GnRH-deficient men. Analysis by gel filtration chromatography revealed that circulating immunoreactive FSH coeluted with radiolabeled authentic FSH. T enanthate treatment suppressed serum FSH levels in each subject from (mean +/- standard error of the mean [SEM]) 1.02 +/- 0.94 to 0.26 +/- 0.21 mIU/ml (P = 0.061, Wilcoxon rank sum test). Thus, FSH is produced in GnRH-deficient men, but there is no evidence for the stimulatory effect of T on FSH production in the absence of GnRH, as observed in the rat. These preliminary data provide further evidence that male contraceptive strategies using GnRH antagonists to suppress LH and FSH production in normal men will not be counteracted by T replacement therapy, although the issue deserves further attention in that study population.
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PMID:FSH is produced by GnRH-deficient men and is suppressed by testosterone. 792 62


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