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PubMed1980

Dopaminergic mechanisms and luteinizing hormone secretion. I. Acute administration of the dopamine agonist bromocriptine does not inhibit luteinizing hormone release in hyperprolactinemic women.

The concept that domapinergic mechanisms control LH secretion by modulation of gonadotropin-releasing hormone (GnRH) has been recently investigated in man. Since hyperprolactinemia is associated with increased hypothalamic dopamine turnover (which may reflect increased dopaminergic activity), inhibition of GnRH by dopamine in this situation would be maximal. Additional stimulation of dopamine receptors by a dopamine agonist would not be expected to result in further inhibition of LH release. Twelve hyperprolactinemic women were studied on 2 days during which measurements of serum PRL and LH were made over 11.5 h. Day 1 served as a control for day 2 when 2.5 mg of the dopamine agonist bromocriptine were administered orally at 0900 h. While serum PRL and LH levels on day 1 showed small fluctuations (+/- 10%), serum PRL on day 2 fell by 82%. Serum LH concentrations on day 2 remained unchanged. The demonstration or the efficacy of bromocriptine in lowering PRL levels documents the expected increase in dopaminergic tone; however, the lack of effect of bromocriptine in surpressing LH release suggests that either there is already maximal endogenous inhibition of GnRH in hyperprolactinemic women or, alternatively, that dopaminergic mechanisms are unimportant in the control of LH secretion.

Adult↗
PubMed1980

Melatonin does not suppress the pituitary luteinizing hormone response to luteinizing hormone-releasing hormone in men.

The effect of an iv melatonin infusion on the pituitary LH response to LHRH was studied in five young men. Melatonin (30 micrograms/min; total dose, 7.2 mg) was infused for a 4-h period, 2 h before and 2 h after a LRH stimulation (single iv 150-microgram dose). Each subject's control response to LRH was obtained previously. During the melatonin infusion, supraphysiological concentrations of melatonin (20 times) were documented using a specific RIA. All five subjects had a LH rise after LRH stimulation, and this response was not affected by the melatonin infusion. These results indicate that an acute constant infusion of a pharmacological amount of melatonin does not suppress LRH-induced LH release from the pituitary in men. In addition, no change in sleepiness and behavior was found.

Adult↗
PubMed1981

Simultaneous pulsatile release of prolactin and luteinizing hormone induced by luteinizing hormone-releasing factor agonist.

Subcutaneous injection of 50 microgram long acting agonist of LRF (LRF-Ag) resulted in the prompt, simultaneous pulsatile release of both LH and PRL in four hypogonadal women. After repeated daily administration of LRF-Ag. LH release in response to LRF-Ag was markedly attenuated, and LH pulses were abolished. LRF-Ag induced PRL release was also attenuated but remained pulsatile. These findings demonstrate the dissociation of the LRF-Ag-induced contemporaneous release of LH and PRL and suggest a hypothalamic site of action of LRF-Ag on PRL release.

Estradiol↗
PubMed1982

Evaluation of pituitary gonadotropic function in men: value of luteinizing hormone-releasing hormone response versus basal luteinizing hormone level for discrimination of diagnosis.

We examined the serum LH response to LRH in 40 normal men and 38 men with various forms of gonadal dysfunction in an attempt to determine whether the LH response to LRH was more useful than the basal LH level alone for categorizing pathophysiological subgroups of gonadal dysfunction. The subgroups studied included hypogonadotropic hypogonadism, delayed puberty, idiopathic oligospermia, and primary hypogonadism. Log transformation of all values was done in order to normalize the data. Spearman's correlation analysis showed that increased basal LH was associated with increased incremental LH responses. However, our preliminary analysis of LRH response data suggested that the changes in LH were smaller in the secondary hypogonadal and delayed puberty groups then could be accounted for by the differences in basal LH level. Accordingly, we used various statistical techniques to test whether, and under what conditions, LRH testing provides information beyond that evident from examination of basal LH values. We found that the relationship between basal LH and the LH response to LRH differs in men with and without hypothalamic-pituitary dysfunction and that this difference can be exploited to improve the discrimination of men with pituitary hypogonadism from normals.

Adolescent↗
PubMed1983

Serum luteinizing hormone and follicle-stimulating hormone and the response to luteinizing hormone-releasing factor in children and adolescents with isolated growth hormone deficiency.

Serum concentrations of LH and FSH were measured in 95 patients (62 males and 33 females) with presumed isolated GH deficiency [chronological age range, 5-17 yr; bone age (BA) range, 2-15.5 yr] before and after the iv administration of 100 micrograms LRF. The results were compared to those of patients of similar skeletal maturity, derived from a population of 136 children (79 males and 57 females) with constitutional short stature. Mean serum LH concentrations were similar in the GH-deficient and control patients of either sex within the age ranges studied. Mean basal FSH concentrations in males with GH deficiency were similar to the controls between BA 2 to less than 10 yr and more than 12 to 15.5 yr. The mean peak, peak minus basal, and integrated responses of LH concentrations after the iv administration of LRF were not significantly different in patients with GH deficiency from the responses in normal short children of similar ages. After LRF administration, GH-deficient males of BA between 2 and less than 10 yr had diminished FSH responses. The mean peak concentration was 1.9 +/- 0.2 ng/ml in GH-deficient males (n = 34) and 2.8 +/- 0.3 ng/ml (less than 0.05) in control males (n = 45). GH-deficient males of BA between 10-12 yr had slightly elevated mean peak and total integrated FSH concentrations; in GH-deficient patients (n = 15), these values were 2.7 +/- 0.2 ng/ml and 2.1 +/- 0.2 ng X min ml-1, respectively; and in controls (n = 18), they were 1.8 +/- 0.2 ng/ml (P less than 0.05) and 1.5 +/- 0.2 ng X min ml-1 (P less than 0.05). In the BA range from 4-8 yr, the mean peak response to LRF was diminished in GH-deficient females (n = 24; 4.0 +/- 0.4 ng/ml) compared to that in control females (n = 18; 6.0 +/- 0.9 ng/ml; P less than 0.05). In the BA range from more than 8 to 13 yr, the corresponding mean peak FSH concentration in GH-deficient females (n = 9) was 3.2 +/- 0.3 ng/ml; in control females (n = 39), it was 4.9 +/- 0.4 ng/ml (P less than 0.05). This study fails to confirm previous reports that LRF-evoked LH release is diminished in patients with isolated GH deficiency compared to that in normal short children of similar skeletal maturity. Small differences in group mean FSH concentrations were noted, but these findings are of limited clinical importance because an extensive degree of overlap of individual FSH concentrations was found in all comparisons between GH-deficient patients and normal children.

Adolescent↗
PubMed1984

Inhibition of serum luteinizing hormone and testosterone with an inhibitory analog of luteinizing hormone-releasing hormone in adult male rhesus monkeys.

The effects of single and repeated administration of a potent LHRH inhibitory analog (antagonist) [( N-acetyl-D-p-chloro-Phe1,2,D-Trp3,D-Arg6,D-Ala10]LHRH) on serum concentrations of LH and testosterone (T) in adult rhesus monkeys were studied. In Exp 1, single sc injections of the LHRH antagonist (400 micrograms and 50 micrograms) or vehicle were administered and the temporal changes in serum LH and T were determined (n = 4 per group). Both LH and T declined markedly in all animals as soon as 30 min after the LHRH antagonist injection, reaching the nadir (80%) approximately 8 h later and remaining significantly lower than baseline levels for up to 24 h. Control animals had no marked variations in either LH or T serum levels. In Exp 2, daily sc injections of different doses of LHRH antagonist (400 micrograms, 50 micrograms, and 10 micrograms) or vehicle were administered for 7 days to four animals in each group. The animals in the control group had no significant changes in LH or T levels, whereas those treated with the lowest dose of LHRH antagonist (10 micrograms) had decreased T levels in the absence of changes in LH. The other two doses of LHRH antagonist (400 micrograms and 50 micrograms) induced, as early as 8 h after the initial injection, dramatic decreases in serum levels of both LH and T and these values remained significantly lower than control for up to 3 and 4 days after discontinuation of drug administration, respectively. We conclude from this study that LHRH inhibitory analogs are potent inhibitors of LH and T in adult rhesus monkeys. They have potential use in clinical trials for male contraception as well as in patients in whom inhibition of gonadotropin and steroid secretion is desired.

Animals↗
PubMed1987

Differential control of luteinizing hormone and follicle-stimulating hormone secretion by luteinizing hormone-releasing hormone pulse frequency in man.

To test the hypothesis that the frequency of pulsatile LHRH stimulation can differentially control LH and FSH secretion in man, we administered low doses of LHRH in pulsatile fashion in several different regimens to men with idiopathic hypogonadotropic hypogonadism (IHH) and presumed endogenous LHRH deficiency. In study 1, four men with IHH received a constant amount of LHRH per day in three different frequencies. After an initial 7-day period of LHRH (5.0 micrograms every 2 h), the men received 2.5 micrograms every 1 h and 7.5 micrograms every 3 h, each for 4 days, in varying order. Frequent blood samples were obtained before LHRH administration and at the end of each regimen. Before LHRH administration, mean serum FSH and LH levels were low [28 +/- 3 (+/- SEM) and 6 +/- 2 ng/mL, respectively], and they increased into the normal adult male range during LHRH treatment. As the frequency of LHRH administration decreased from every 1 to 2 to 3 h, serum FSH levels progressively increased from 99 +/- 33 to 133 +/- 34 to 181 +/- 58 ng/mL (P less than 0.05). Serum LH levels (34 +/- 6, 33 +/- 6, and 34 +/- 5 ng/mL) were significantly higher than those before LHRH administration and did not differ significantly among the three regimens. Total serum testosterone (T), estradiol, and free T levels were increased by LHRH, but were not significantly different during the three regions of LHRH administration. In study 2, three men with IHH received the same amount of LHRH per dose, given in two different pulse frequencies; 2.5 micrograms LHRH were administered in frequencies of every 0.5 h and every 1.5 h, each for 4 days, in varying order. During the 0.5 h frequency, the mean serum FSH level was 42 +/- 13 ng/mL, and it rose to 80 +/- 19 ng/mL during the 1.5 h frequency (P less than 0.05). Corresponding mean serum LH levels were 25 +/- 5 and 27 +/- 4 ng/mL. Serum T and estradiol levels were not significantly different during the two LHRH regimens. We conclude that the frequency of LHRH stimulation can differentially control FSH and LH secretion by the human pituitary gland, and the pattern of hormonal stimulation may be a determinant of target organ response.

Adult↗
PubMed1995

Pharmacokinetics of recombinant human luteinizing hormone after intravenous, intramuscular, and subcutaneous administration in monkeys and comparison with intravenous administration of pituitary human luteinizing hormone.

To assess the pharmacokinetics of recombinant human LH (rhLH) in monkeys, we measured serum LH levels after single iv injection and after single and repeated doses by the im or sc route. A single iv bolus of 400 IU/kg rhLH or pituitary hLH (phLH) in six cynomolgus monkeys resulted in parallel concentration-time curves. The initial and terminal half-lives of rhLH (0.8 and 11 h) were comparable to those of phLH (0.6 and 10 h). The serum levels of phLH were consistently higher due to the fact that the immunological dose of phLH was higher. Administration of increasing iv doses of rhLH (10, 63, and 400 IU/kg) to six monkeys showed that the pharmacokinetics are linear over this dose range. The total clearance for the two higher doses was 0.03 L/h.kg. Systemic bioavailability was 50% after a single sc injection of 400 IU/kg and 61% after a single im injection of the same dose. The peak concentration (180 IU/L) after im injection was reached after 2.7 h. This was higher and sooner than after sc injection (110 IU/L after 5.3 h). The terminal half-life by both routes was similar to that seen after iv injection (11 h). Daily sc or im administration of 63 IU/kg for 7 days confirmed these findings. There was no accumulation of rhLH. Some monkeys developed antibodies, especially after repeated administration. They were excluded from the analysis. No significant local or systemic adverse events occurred.

Animals↗
PubMed1988

Stimulation of pituitary luteinizing hormone secretion by gonadotropin-releasing hormone is not coupled to beta-luteinizing hormone gene transcription.

The physiological stimulation and inhibition of release of several peptide and protein hormones appears to be associated with transcription of the respective peptide- and protein hormone-encoding genes. In the current studies we investigated whether this was also true for the rat pituitary LH system. Using an anterior pituitary primary tissue culture system, we have analyzed the effects of 10(-9) M GnRH on beta LH gene transcription using a transcription run-on assay, and on nuclear beta LH RNA levels using a highly sensitive solution hybridization-S1-nuclease protection assay. GnRH-stimulated release of LH does not appear to be coupled to a significant change in the rate of beta LH gene transcription, but is associated with both a 2- to 3-fold increase in levels of the beta LH primary transcript and processing intermediates and a rapid decrease in the levels of fully processed beta LH mRNA in the nucleus. No significant change in beta LH cytoplasmic mRNA levels, however, was associated with GnRH-stimulated release of LH, in vitro. Our findings suggest that unlike several other peptide and protein hormone systems, stimulated release of beta LH by GnRH in vitro is not associated with an increase in beta LH gene transcription or cytoplasmic mRNA levels.

Animals↗
PubMed1990

Hormonal regulation of luteinizing hormone/chorionic gonadotropin receptor mRNA in rat ovarian cells during follicular development and luteinization.

To determine whether hormone-dependent changes in the levels of LH/CG receptor in the rat ovary are associated with changes in expression of LH/CG receptor mRNAs, total RNA from rat follicles and corpora lutea at various stages of development was prepared and analyzed by Northern blots and/or solution hybridization. Whereas small antral follicles contained lo amounts of LH/CG receptor mRNAs, the growth of preovulatory (PO) follicles was associated with an increase in all LH/CG receptor mRNA transcripts. Induction of LH/CG receptor mRNAs in granulosa cells of hypophysectomized rats was dependent on the synergistic effects of estradiol and FSH. An LH/CG surge in vivo or LH treatment of PO follicles in vitro caused a rapid decline of all LH/CG receptor mRNAs in PO follicles, which was prevented by cycloheximide. Newly formed corpora lutea (days 1-4 postovulation) contained low amounts of LH/CG receptor mRNAs unless the rats were pregnant or treated exogenously with PRL. During pregnancy, corpora lutea isolated on days 4-19 of gestation contained high levels of LH/CG receptor mRNAs, which decreased markedly on days 21 and 24, the time of functional luteolysis and decreasing LH/CG receptor levels. These studies demonstrate that hormonal regulation of LH/CG receptor mRNA in rat ovarian cells parallels changes in LH/CG receptor levels and involves diverse molecular mechanisms, including 1) low concentrations of cAMP (elicited by FSH) in developing follicles, 2) inhibition by high concentrations of cAMP (elicited by LH/CG) in PO follicles, and 3) induction and maintenance by PRL in corpora lutea of gestation.

Animals↗
PubMed1982

Biological and immunological characterization of human luteinizing hormone discharged by the stimulation of synthetic luteinizing hormone-releasing hormone (LH-RH) in normal and anovulatory women.

Plasma samples were obtained by repeated venopunctures immediately before, and at 15, 30, 60, 120 and 180 min after intravenous bolus administration of 100 micrograms synthetic LH-RH in normal and various anovulatory women. Plasma hLH levels were determined by an in vitro bioassay and a radioimmunoassay with improved reagents. The LH-RH stimulation induced an abrupt elevation of both biological and immunological hLH activities in normal and anovulatory women, although the responsiveness to LH-RH differed from case to case. Both elevated biological and immunological hLH activities decreased gradually with a half disappearance time of 122.4 +/- 27.9 min and 112.5 +/- 25.4 min, respectively (Mean +/- S.D.). A transient and significant depression in the ratio of biological to immunological hLH activities (B/I ratio) was observed at 15 min after the LH-RH administration in normal subjects. This depression is attributable to the cross-contamination of an increased amount of hLH subunits induced by LH-RH stimulation. The B/I ratios were significantly elevated throughout the investigation period in the anovulatory patients when compared with those in the normal subjects. This elevation appears to indicate the increased discharge of special type(s) of hLH subpopulations of high biological potency in the anovulatory cases.

Adult↗