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

Two experiments were conducted: 1) to assess the ovulation-blocking ability and steroidogenesis-inhibiting activity of aminoglutethimide in the laying hen; and 2) to determine whether LHRH or progesterone (P4) administration can overcome the ovulation-blocking effect of aminoglutethimide. Aminoglutethimide inhibited ovulation and suppressed the secretion of P4 and testosterone (T) in a dose-related fashion. In the absence of any increase in plasma P4 and T, there was no preovulatory increase in plasma LH. These results indicate that the preovulatory surge of LH is initiated by an increase in steroid. The effectiveness of P4 and LHRH to stimulate LH release and overcome the ovulation-blocking effect of aminoglutethimide was tested in the second experiment. Administration of 500 micrograms P4 (im) to aminoglutethimide-treated hens resulted in a significant and sustained release of LH [peak, 3.08 +/- 0.62 (+/- SEM) ng/ml; 120 min after injection] and induced ovulation in the absence of any increase in plasma T or estrogen. In contrast, injection of 20 micrograms LHRH (iv) failed to overcome the blocking effect of aminoglutethimide and caused an attenuated (peak, 2.17 +/- 0.37 ng/ml; 60 min after injection) and short-lived increase in plasma LH. These results are consistent with the model for a true positive feedback mechanism in which P4 initiates and sustains the preovulatory LH surge of the hen.
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PMID:Effects of aminoglutethimide on luteinizing hormone and steroid secretion, and ovulation in the hen, Gallus domesticus. 637 41

The luteinizing hormone releasing hormone analog D-Trp6-Pro9-Net-LHRH (LHRHa) inhibits rat testicular testosterone secretion. To determine whether LHRHa decreases serum testosterone concentrations solely by inhibiting gonadotropin secretion or, in addition, by influencing directly testicular testosterone biosynthesis, we examined the effects of LHRHa on the activities of 5 key testicular steroidogenic enzymes. Thirty hypophysectomized, hOG treated rats were given either LHRHa (1 micrograms sc/day) or saline during 7 days. The LHRHa treated animals exhibited a significant decrease of serum testosterone when compared to the control group (498 +/- 37 ng/dl vs 2044 +/- 105 ng/dl, mean +/- SEM, P less than 0.001). 17-Hydroxyprogesterone serum levels were also decreased in the LHRHa treated rats (61 +/- 6 ng/dl vs 93 +/- 7 ng/dl, P less than 0.005), while serum progesterone levels were similar in both groups of animals. These changes in steroid concentrations were associated with decreases in the microsomal enzyme activities of 17-hydroxylase (37 +/- 9 vs 654 +/- 41 pmol/mg protein/min, P less than 0.001), 17,20-desmolase (103 +/- 9 vs 522 +/- 47 pmol/mg protein/min, P less than 0.001), 3 beta-hydroxysteroid dehydrogenase (1.7 +/- 0.02 vs 4.1 +/- 0.1 nmol/mg protein/min, P less than 0.001), aromatase (95 +/- 7 vs 228 +/- 6 pmol/mg protein/min, P less than 0.001) and 17-ketosteroid reductase (167 +/- 9 vs 290 +/- 18 pmol/mg protein/min, P less than 0.01) in the LHRHa treated animals. These findings indicate that LHRHa can inhibit directly rat testicular testosterone biosynthesis.
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PMID:Direct effect of the luteinizing hormone releasing hormone analog D-Trp6-Pro9-Net-LHRH on rat testicular steroidogenesis. 639 51

In experimental animals, primary testicular deficiency leads to increased LH pulse frequency. Pulsatile FSH secretion has not been well characterized in any species. To determine the effect of testosterone (T) on the pattern of pulsatile gonadotropin secretion in man, we performed frequent blood-sampling studies in six normal men and six men with primary hypogonadism. All primary hypogonadal men were studied 6-8 weeks after stopping T replacement therapy. Five of the six hypogonadal men were restudied 6-8 weeks after treatment with T enanthate (200 mg, im, every 2 weeks; sampling in this group was 2 weeks after their last T injection). Blood sampling was done at 10-min intervals for 12 h in all subjects, and the pattern of episodic LH and FSH secretion was determined. Normal men had a serum T level of 6.3 +/- 0.3 ng/ml (mean +/- SEM), a LH level of 34 +/- 3 ng/ml, and a LH pulse pattern characterized by low frequency (7.6 +/- 0.7 pulses/12 h) and low amplitude (16 +/- 1 ng/ml). Compared to normal men, primary hypogonadal men had a significantly lower T level (2.9 +/- 0.4 ng/ml) and significantly higher LH pulse frequency (13.0 +/- 1.3 pulses/12 h), amplitude (51 +/- 7 ng/ml), and mean level (222 +/- 26 ng/ml). Reinstitution of T replacement therapy in hypogonadal men resulted in a significant increase in the T level (4.7 +/- 0.5 ng/ml) and significant decreases in LH pulse frequency (7.2 +/- 1.6 pulses/12 h) and amplitude (41 +/- 5 ng/ml) as well as mean LH level (75 +/- 15 ng/ml). FSH levels fluctuated in a distinctly pulsatile pattern in all three groups. Differences in pulsatile FSH secretion between primary hypogonadal men before and during T therapy and normal men paralleled those in pulsatile LH secretion in both frequency and amplitude. These results demonstrate that in man 1) diminished T negative feedback results in high frequency (circhoral), high amplitude LH and FSH pulses; 2) T replacement decreased LH and FSH pulse frequency and amplitude as well as mean levels; and 3) the decreased LH and FSH pulse frequency with T treatment implies that T or a metabolite of T acts on the central nervous system to slow the hypothalamic LHRH pulse generator.
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PMID:Modulation of pulsatile gonadotropin secretion by testosterone in man. 642 64

Synthetic, amidated, 44 amino acid GH-releasing hormone ( GRH -44) was administered iv at a dose of 5 micrograms/kg to 20 patients with severe GH deficiency (GHD), 6 children and adolescents with partial GHD, and 6 non-GH deficient ( NGHD ) children and adolescents. The 17 patients with severe GHD that responded to GRH -44 had lower peak concentrations of plasma GH than the NGHD individuals (5.0 +/- 1.2 (SEM) vs. 27.2 +/- 3.5 ng/ml; P less than 0.0001). The children and adolescents with severe GHD tended to have higher peak GH responses to GRH -44 than the GHD adults (6.9 +/- 1.7 vs. 2.4 +/- 0.3 ng/ml) although the difference was not significant. The peak GH concentration was attained earlier in the GHD children and adolescents than in the GHD adults (28 +/- 4.7 vs. 69.3 +/- 13 min, P less than 0.004). There was a negative correlation between chronological age and peak plasma GH response to GRH in the children and adolescents with severe GHD (r = -0.758, P less than 0.02). Children and adolescents with partial GHD had a higher mean peak concentration of plasma GH (13. 1 +/- 1.8 ng/ml) than the children, adolescents, and adults with severe GHD (P less than 0.04), but one lower than the NGHD children and adolescents (P less than 0.05). In both severe and partial GHD the GH response to GRH was greater than that elicited by standard pharmacological tests. Serum somatomedin-C did not increase after a single pulse of GRH -44 in the 12 GHD patients studied. PRL increased minimally 30 min after 5 micrograms/kg iv GRH -44 in patients with multiple hypothalamic-pituitary hormone deficiencies but not in patients with isolated GHD or in NGHD individuals. The GH responses to GRH suggest that the majority of patients with isolated GHD as well as those with multiple hypothalamic-pituitary hormone deficiencies have deficiency of hypothalamic GRH . Lack of a GH response to a single pulse of GRH does not exclude GRH deficiency as priming of the somatotrope with multiple pulses of GRH may be necessary to rule out a hypothalamic defect in the nonresponders. The results of this study support the potential usefulness of GRH or its analogs in the diagnosis and treatment of selected patients with disorders of GH secretion.
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PMID:Effect of growth hormone (GH)-releasing hormone (GRH) on plasma GH in relation to magnitude and duration of GH deficiency in 26 children and adults with isolated GH deficiency or multiple pituitary hormone deficiencies: evidence for hypothalamic GRH deficiency. 642 57

This study was designed to determine whether the lack of secretion of endogenous gonadotropin-releasing hormone is the etiology of the hypogonadotropic state of pregnancy. For this purpose, five pregnant women in their first trimester received a single intravenous dose of 150 micrograms of gonadotropin-releasing hormone. Another five women in the first trimester and five women in the second trimester of pregnancy received daily intramuscular injections of 500 micrograms of gonadotropin-releasing hormone for 10 consecutive days. This was followed by a single 150 micrograms gonadotropin-releasing hormone test and then a 24-hour pulsatile infusion of gonadotropin-releasing hormone of 10 micrograms/min/6 min given every hour. Baseline plasma beta-luteinizing hormone and follicle-stimulating hormone were undetectable in all women. Mean +/- SEM plasma beta-human chorionic gonadotropin was significantly higher (p less than 0.001) in the first trimester than in the second trimester, and mean plasma estradiol and prolactin were significantly increased (p less than 0.001 and 0.05, respectively) during the second trimester of pregnancy. After the 10-day treatment with gonadotropin-releasing hormone there was a significant increase (p less than 0.05) in baseline beta-luteinizing hormone and follicle-stimulating hormone only in the first-trimester pregnant women. The single as well as the pulsatile administration of gonadotropin-releasing hormone resulted in a further significant increase in both beta-luteinizing hormone and follicle-stimulating hormone. In contradistinction, women in the second trimester of pregnancy showed a blunted response to the daily and pulsatile administration of gonadotropin-releasing hormone. Since the pituitary secretion of gonadotropin was functionally restored by the administration of exogenous gonadotropin-releasing hormone, possibly there is a lack of secretion of endogenous gonadotropin-releasing hormone during the first trimester of pregnancy. An increased negative feedback produced by increasing levels of plasma estradiol might be the cause of pituitary refractoriness to gonadotropin-releasing hormone during the second trimester of pregnancy.
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PMID:Priming with gonadotropin-releasing hormone restores gonadotropin secretion during first but not second trimester of pregnancy. 643 25

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

Optimum conditions for a sensitive and highly precise radioimmunoassay of LHRH were established. Precipitation and removal of interfering substances and concentration of the resultant LHRH extracts from peripheral plasma were also achieved. Using these methods, daily plasma LHRH levels in females with normal menstrual cycles were measured and correlated with the corresponding LH and FSH levels. The levels of LHRH in the peripheral plasma of postmenopausal females, as well as eugonadal males, were also determined. The LHRH profile in normal cycling women was found to be cyclic but the peak LHRH levels were observed at the beginning of the rise in LH and FSH levels and preceded the midcycle surge of gonadotrophins. The LHRH levels in the luteal phase (19.8 +/- 1.1 pg/ml, mean +/- SEM) were significantly (P less than 0.01) higher than those in the follicular phase (16.5 +/- 0.5 pg/ml) of the menstrual cycle. A high degree of correlation (r = 0.91) was seen between the immunoreactivity and biological activity of the extracted LHRH.
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PMID:Inter-relationship between changing patterns of LHRH and gonadotrophins in the menstrual cycle. 679 4

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

A gonadotropin-releasing hormone (GnRH) was injected in mares given prostaglandin F2 alpha (PGF2 alpha) to induce luteolysis in an attempt to sunchronize ovulation. Pretreatment with estradiol-17 beta (E2-17 beta) was used to determine whether or not estradiol would enhance the release of luteinizing hormone (LH) after treatment with GnRH. Twelve mares were used in a balanced Latin square crossover design. Mares were injected with PGF2 alpha, treatment A; PGF2 alpha mgnRH, treatment B; or PGF2 alpha me2-17 beta mgnRH, treatment C. The interval +/- SEM from PGF2 alpha injection to estrus was 3.3 +/- 0.2, 3.2 +/- 0.3, and 2.3 +/- 0.1 days for treatments A, B, and C, respectively. The mean interval in days from injection to first ovulation averaged 1 day less (P less than 0.10) for treatments B (6.7 +/- 0.6) and C (6.2 +/- 0.3) than for treatment A (7.6 +/- 0.7). The furation of estrus and the interval from ovulation to end of estrus were similar among the three treatment groups. Mares treated with GnRH (treatments B and C) had a significant (P less than 0.01) two- to threefold increase in LH concentrations when compared with controls. Pretreatment with estradiol-17 beta did not appear to enhance LH release after GnRH was given, and the time of ovulation was not significantly changed by GnRH treatment.
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PMID:Estrus, ovulation, and serum hormones in mares given prostaglandin F2 alpha, estradiol, and gonadotropin-releasing hormone. 698 21


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