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PubMed1977

Gonadotrophin release by a highly active analogue of luteinizing hormone releasing hormone in rats immunized against luteinizing hormone releasing hormone.

Immunization against luteinizing hormone releasing hormone (LH-RH) in adult male rats produced a progressive decline in LH and FSH in the circulation to low or non-detectable levels. D-Serine-tertiary-butyl6,des-glycine-NH210 LH-RH ethylamide is an analogue of LH-RH having highly active LH-RH properties in the normal rat. Because it is also immunologically different from LH-RH it can stimulate gonadotrophin release from the anterior pituitary gland of rats immunized against LH-RH without interference from the antibody. The analogue stimulated LH and FSH release in rats 15 weeks after immunization against LH-RH when antibody titre was highest, and after long-term (35 weeks) immunization against LH-RH. D-Serine-tertiary-butyl6,des-glycine-NH210 LH-RH ethylamide and related analogues are therefore potentially useful for reversing the effects of immunization against LH-RH.

Animals↗
PubMed1979

Differential control of luteinizing hormone and follicle-stimulating hormone by luteinizing hormone releasing hormone in the ram.

Adult Soay rams with low concentrations of gonadotrophins in the circulation as a result of 12 weeks of exposure to long daylengths (16 h light : 8 h darkness) were given small doses (100 ng) of synthetic luteinizing hormone releasing hormone (LH-RH) into the jugular vein two, four or seven times/day for 10 days. Each injection of LH-RH induced a transitory increase in the concentration of LH and testosterone in the plasma, whereas the concentration of FSH showed little immediate change. After repeated treatment with pulses of LH-RH, the responses of LH and testosterone became slightly enhanced and the plasma concentration of FSH became permanently raised; these changes were most conspicuous in the animals receiving the most frequent injections. At the end of the study when the injections of LH-RH were stopped, the concentrations of LH and testosterone remained low but the concentrations of FSH continued to be maintained at a high level for at least 24 h.

Animals↗
PubMed1983

Luteinizing hormone releasing hormone prevents testicular atrophy in golden hamsters exposed to a short photoperiod: temporal difference in effectiveness of administration of luteinizing hormone releasing hormone.

Exposure of male golden hamsters to short photoperiods of 6 h light: 18 h darkness led to testicular and accessory sex organ atrophy in 5 weeks. Short photoperiods also significantly depressed serum levels of LH, FSH, prolactin and testosterone in samples obtained by decapitation, but not in samples collected on the preceding day under ether anaesthesia. Injections of luteinizing hormone releasing hormone (LH-RH) at 09.00 h (lights on) or at 15.00 h (lights off) prevented testicular regression when compared with hamsters receiving injection vehicle only. However, the hamsters receiving LH-RH injections at lights on had significantly greater testicular weight and accessory sex organ (seminal vesicles and coagulating glands) weight and testosterone concentration than those receiving LH-RH at lights off. No increase in testicular weight was observed in hypophysectomized male hamsters given the same LH-RH injections and the same lighting regimen. These results indicate that LH-RH alone can prevent, at least partially, testicular and sex organ atrophy and increase serum testosterone concentration by stimulating release of LH and FSH in hamsters exposed to short photoperiods, involving temporal difference of LH-RH action. Further implications of the results are discussed.

Animals↗
PubMed1991

Growth hormone secretion in aging. Effect of pyridostigmine on growth hormone responsiveness to growth hormone-releasing hormone.

Recent studies in adults have shown that cholinergic enhancement by pyridostigmine (PD) has a stimulatory effect on growth hormone (GH) response to GH-releasing hormone (GHRH). PD probably reduces somatostatin release from the hypothalamus by increasing the central cholinergic tone. The aim of this study was to evaluate the effect of PD (120 mg orally) or placebo pretreatment on GH responsiveness to GHRH (1 micrograms/kg b.w. i.v.) or placebo in 10 normal elderly males (68-92 years). PD induced a significant increase in GH secretion (GH peak 7.3 +/- 1.8 micrograms/L, mean +/- SEM) over the basal value (0.9 +/- 0.2 micrograms/L; P less than 0.01) and enhanced GH response to GHRH (peak after GHRH: 17.0 +/- 3.8 micrograms/L; after PD plus GHRH: 42.6 +/- 12.2 micrograms/L; P less than 0.05). There was a significant difference in the secretory areas of GH among tests (P less than 0.05). The secretory area was greater after PD plus GHRH (2722 +/- 801 micrograms/L/120 min) than after GHRH (1185 +/- 206 micrograms/L 120 min; P less than 0.01). The effect of PD on GH secretion suggests that cholinergic mechanisms may be involved in GH control in normal aging. During the life-span cholinergic neurons and/or the somatostatin pathways could exert a differential effect on GH control.

Aged↗
PubMed1993

The value of urinary growth hormone determination for assessment of growth hormone deficiency and compliance with growth hormone therapy.

OBJECTIVE: To compare the 24-hour integrated concentrations of plasma growth hormone with growth hormone levels in a simultaneously collected sample of urine. SETTING: Pediatric endocrine diagnostic unit. PATIENTS: Forty-six children (41 male and five female) aged 6 to 19 years underwent measurement of integrated concentrations of growth hormone and simultaneous urine collection. MEASUREMENTS AND RESULTS: Integrated concentration of plasma growth hormone was correlated with urinary growth hormone levels from both the 24-hour (r = .67; P < .0001) and 12-hour overnight (r = .52; P < .001) measurements. Peak growth hormone response to paired stimulation was not correlated with either the 24-hour (r = .26; P < .23; n = 28) or 12-hour (r = .16; P < .48; n = 28) urinary growth hormone levels. The mean 24- and 12-hour urinary growth hormone levels for the patients with normal integrated concentrations of growth hormone were significantly higher than those in patient groups having subnormal integrated concentrations of growth hormone (P < .05). However, there was considerable overlap in the 12- and 24-hour urinary growth hormone levels between the patients with normal and those with subnormal integrated concentrations of growth hormone. Only one patient who had subnormal integrated concentrations of growth hormone had a 24-hour urinary growth hormone level higher than 9 ng, and none had a 12-hour urinary growth hormone level higher than 7 ng. The mean 12- and 24-hour urinary growth hormone levels were significantly higher in patients who received growth hormone injection than in those with normal spontaneous integrated concentrations of growth hormone and had no overlap with patients who had subnormal integrated concentrations of growth hormone. CONCLUSIONS: (1) Urinary and integrated concentrations of plasma growth hormone are correlated; (2) patient diagnoses based on integrated plasma growth hormone levels exhibit a high degree of overlap of urinary growth hormone; and (3) urinary growth hormone levels can serve to monitor compliance with growth hormone therapy.

Adolescent↗
PubMed1989

Differential role of protein kinase C in the action of luteinizing hormone-releasing hormone on hormone production in rat ovarian cells.

This study was undertaken to determine the involvement of arachidonic acid and protein kinase C in the actions of luteinizing hormone-releasing hormone on steroid and prostaglandin formation in the ovary. In primary culture of rat granulosa cells, treatment with 3 x 10(-7) mol/L melittin stimulates progesterone and prostaglandin E2 accumulation after a 5-hour culture period. Concomitant treatment of the cells with melittin and luteinizing hormone-releasing hormone or 12-0-tetradecanoylphorbol 13-acetate further enhances the stimulatory action of either luteinizing hormone-releasing hormone or 12-0-tetradecanoylphorbol 13-acetate by itself on prostaglandin E2 production. In contrast, no synergistic effects are observed on progesterone production by the same treatments. Treatment with luteinizing hormone-releasing hormone for 24 hours significantly decreases follicle-stimulating hormone-induced progesterone production by approximately 50%. Treatment of the cells with either follicle-stimulating hormone or luteinizing hormone-releasing hormone stimulates prostaglandin E2 production at least tenfold in the same cultures. When follicle-stimulating hormone and luteinizing hormone-releasing hormone are present concomitantly, they synergistically enhance prostaglandin E2 formation (p less than 0.01). Similar effects are observed with the phorbol ester, 12-0-tetradecanoylphorbol 13-acetate, which causes a dose-dependent inhibition of progesterone production by follicle-stimulating hormone whereas follicle-stimulating hormone-stimulated prostaglandin E2 formation is enhanced. Thus luteinizing hormone-releasing hormone-induced activation of protein kinase C may play multiple roles (stimulatory or inhibitory) in hormone production in the ovary.

Animals↗
PubMed1996

Effects of growth hormone and growth hormone-releasing hormone on steroid synthesis in cultured human luteinizing granulosa cells.

To assess the direct effect of growth hormone and growth hormone-releasing hormone on gene expression of steroidogenic enzymes and production of progesterone, 17-hydroxyprogesterone (17-OHP) and estradiol, we cultured luteinizing granulosa cells with or without follicle-stimulating hormone (FSH), growth hormone and growth hormone-releasing hormone at different concentrations. Luteinizing granulosa cells were obtained from women undergoing an in vitro fertilization program in the Department of Obstetrics and Gynecology, S. Raffaele Scientific Institute, Milan, Italy. At a concentration of 1 microgram/ml, FSH significantly increased estradiol production (2.1 +/- 0.7-fold the control value; p < 0.05 vs. control) and progesterone production (3.5 +/- 2.0-fold the control value; p < 0.05 vs. control). Growth hormone was effective on estradiol, progesterone and 17-OHP at 1 microgram/ml, enhancing estradiol production (1.3 +/- 0.2-fold the control value; p < 0.05 vs. control), progesterone production (2.5 +/- 1.0-fold the control value; p < 0.05 vs. control), and 17-OHP (1.4 +/- 0.2-fold the control value; p < 0.05 vs. control). Growth hormone-releasing hormone increased estradiol production (1.5 +/- 1.2-fold the control value) and progesterone production (1.3 +/- 0.8-fold the control value), but not significantly. No effects by growth hormone-releasing hormone were seen on 17-OHP production. FSH, growth hormone and growth hormone-releasing hormone did not increase P450scc and P450 aromatase mRNAs, whereas FSH increased P450c17 mRNA to 150% at 100 ng/ml and 1 microgram/ml, growth hormone increased it to 230% at 100 ng/ml and to 200% at 1 microgram/ml, and growth hormone-releasing hormone increased it to 140% at 100 ng/ml and to 190% of control values at 1 microgram/ml. These results indicate a direct effect of growth hormone on steroidogenesis by increasing P450c17 mRNA accumulation and progesterone, 17-OHP and estradiol production.

17-alpha-Hydroxyprogesterone↗
PubMed1997

Regulation of growth hormone-releasing hormone and somatostatin from perifused, bovine hypothalamic slices. III. Reciprocal feedback between growth hormone-releasing hormone and somatostatin.

An in vitro perifusion system for bovine hypothalamic tissue was used to determine if growth hormone-releasing hormone (GHRH) and somatostatin (SRIF) modulate each other's release, and whether SRIF mediates D1-agonist-induced suppression of GHRH in cattle. Up to three sagittal slices (600 microns) of bovine hypothalamus, immediately parallel++ to the midline, were cut in an oxygenated balanced salt solution at 4 degrees C, placed in 5 cc syringe barrels, and perifused at 37 degrees C with oxygenated minimum essential medium-alpha at a flow rate of 0.15 ml/min. Three experiments were conducted, and medium effluent was collected every 20 min before (two samples), during (one or three samples), and after (six samples) treatment. Areas under GHRH and SRIF response curves (AUC), adjusted by covariance for pretreatment values, were calculated from samples collected during the treatment/post-treatment period. Perifusion of SRIF at 10(-6) M and 10(-4) M decreased AUC for GHRH from 86.3 (control) to 65.4 and 59.5 +/- 6.3 ng.ml-1 min, but 10(-8) M SRIF was ineffective. Relative to controls, 10(-8).10(-6), and 10(-4) M GHRH increased release of SRIF 190, 675, and 1,135%, respectively. Activation of D1 receptors with 10(-6) M SKF 38393 increased AUC for SRIF from 12.5 ng.ml-1 min (control) to 484.9 ng.ml-1 min and decreased AUC for GHRH from 36.4 ng.ml-1 min (control) to 18.2 ng.ml-1 min. Blockade of SRIF action with a SRIF antagonist, cyclo-[7-aminoheptanoyl-phe-D-trp-lys-thr(bzl)], increased release of GHRH 1.9-fold. In addition, the SRIF antagonist blocked SKF 38393-induced suppression of GHRH. We concluded that GHRH and SRIF interact within the bovine hypothalamus/pituitary stalk to modulate the release of the other. Moreover, SRIF mediates the inhibitory effects of activation of D1 receptors on release of GHRH in cattle.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1987

Effect of growth hormone releasing hormone on growth hormone secretion in type 2 (non-insulin-dependent) diabetes mellitus.

Growth hormone levels following an intravenous bolus injection of 1 micrograms/kg body weight growth hormone releasing hormone were measured in 21 non-obese and 26 obese patients with Type 2 (non-insulin-dependent) diabetes mellitus and in 13 control subjects. Growth hormone responses in non-obese Type 2 diabetic patients were not statistically different from control subjects. However, obese Type 2 diabetic patients had significantly decreased growth hormone responses to growth hormone releasing hormone when compared with non-obese Type 2 diabetic patients (p less than 0.02). In 9 Type 2 diabetic patients growth hormone releasing hormone tests were performed both during hyperglycaemia and after metabolic improvement by insulin treatment. Growth hormone responses before and after insulin treatment were not statistically different. Our data demonstrate that growth hormone responses to growth hormone releasing hormone in non-obese Type 2 diabetic patients do not differ significantly from control subjects; obesity blunts growth hormone responses to growth hormone releasing hormone in Type 2 diabetes mellitus; and growth hormone responses following growth hormone releasing hormone administration in Type 2 diabetes mellitus are not influenced by the state of metabolic control.

Aged↗
PubMed2002

Growth hormone response to a novel growth hormone-releasing tripeptide in horses: interaction with gonadotropin-releasing hormone, thyrotropin-releasing hormone, and sulpiride.

A series of experiments was performed to determine the factor(s) responsible for an apparent inhibition of GH secretion in mares administered the GH secretagogue EP51389 in combination with GnRH, thyrotropin-releasing hormone (TRH), and sulpiride. Experiment 1 tested the repeatability of the original observation: 10 mares received EP51389 at 10 microg/kg BW; five received TRH (10 microg/kg BW), GnRH (1 microg/kg BW), and sulpiride (100 microg/kg BW) immediately before EP51389, and five received saline. The mixture of TRH, GnRH, and sulpiride reduced (P = 0.0034) the GH response to EP51389, confirming the inhibitory effects. Experiment 2 tested the hypothesis that sulpiride, a dopamine antagonist, was the inhibitory agent. Twelve mares received EP51389 as in Exp. 1; six received sulpiride before EP51389 and six received saline. The GH responses in the two groups were similar (P > 0.1), indicating that sulpiride was not the inhibitory factor. Experiment 3 tested the effects of TRH and(or) GnRH in a 2 x 2 factorial arrangement of treatments. Three mares each received saline, TRH, GnRH, or the combination before EP51389 injection. There was a reduction (P < 0.0001) in GH response in mares receiving TRH, whereas GnRH had no effect (P > 0.1). Given those results, Exp. 4 was conducted to confirm that TRH was inhibitory in vivo as opposed to some unknown chemical interaction of the two compounds in the injection solution. Twenty mares received TRH or saline and(or) EP51389 or saline in a 2 x 2 factorial arrangement of treatments. Injections were given separately so that the two secretagogues never came in contact before injection. Again, TRH reduced (P < 0.0001) the GH response to EP51389. In addition, TRH and EP51389 each resulted in a temporary increase in cortisol concentrations. Experiment 5 tested whether TRH would alter the GH response to GHRH itself. Twelve mares received porcine GHRH at 0.4 microg/kg BW; six received TRH prior to GHRH and six received saline. After adjustment for pretreatment differences between groups, the GHRH-induced GH response was completely inhibited (P = 0.068) by TRH. Exp. 6 was a repeat of Exp. 5, except geldings were used (five per group). Again, pretreatment with TRH inhibited (P < 0.0001) the GH response to GHRH. In conclusion, TRH inhibits the GH response not only to EP51389 but also to GHRH in horses, and in addition to its known secretagogue action on prolactin and TSH it may also stimulate ACTH at the dosage used in these experiments.

Animals↗
PubMed1984

Hormonal regulation of the growth hormone gene. Relationship of the rate of transcription to the level of nuclear thyroid hormone-receptor complexes.

Using cultured GH1 cells, we reported that stimulation (3- to 5-fold) of growth hormone synthesis and mRNA levels by thyroid hormone is mediated by a chromatin-associated receptor. Thyroid hormone also elicits a rapid reduction of homologous receptor in GH1 cells primarily by decreasing the synthetic rate of receptor ( Raaka , B. M., and Samuels , H. H. (1981) J. Biol. Chem. 256, 6883-6889). Without 3,5,3'-triiodo-L-thyronine (L-T3), glucocorticoid agonists induced a limited and delayed effect while L-T3 + glucocorticoid synergistically stimulated the response an additional 2- to 4-fold compared to L-T3. In this study, we utilized GC cells, a related cell line, to compare the abundance of L-T3-receptor complexes to the rate of growth hormone mRNA synthesis and gene transcription. Gene transcription was assessed by in vitro labeling of nuclei with [alpha-32P]UTP which were derived from cells incubated with hormone(s), while mRNA synthesis was determined in intact cells by [3H]uridine labeling. Labeled growth hormone mRNA and gene transcripts were quantitated by filter hybridization to plasmid containing growth hormone cDNA. L-T3 rapidly decreased receptor levels in GC cells with kinetics similar to that in GH1 cells. Both the L-T3 and the synergistic L-T3 + glucocorticoid stimulation of growth hormone mRNA synthesis changed in parallel with the level of L-T3-receptor complexes. Glucocorticoid hormones alone elicited a variable response which resulted in minimal stimulation or inhibition of growth hormone mRNA synthesis or gene transcription rates. No apparent lag was identified between the kinetics of L-T3 binding to receptor and stimulation of growth hormone gene transcription. L-T3 stimulated growth hormone gene transcription rates maximally in 1 h which then progressively decreased in parallel with L-T3-receptor levels. Using [3H]uridine pulse-chase, growth hormone mRNA was found to have a half-life of approximately 50 h in agreement with the decay curve of growth hormone production of deinduced cells. Our studies suggest that regulation of the growth hormone response is predominantly determined by positive control of growth hormone gene transcription which is proportional to the concentration of thyroid hormone-receptor complexes.

Animals↗
PubMed1975

Response of luteinizing hormone and follicle-stimulating hormone to different doses of synthetic luteinizing hormone-releasing hormone by intramuscular administration in normal and oligospermic men: preliminary report.

The response of LH and FSH levels to intramuscularly administered synthetic LH-RH was studied in two healthy volunteers and three oligospermic patients. Four tests with 50, 100, 250, and 500 mug of LH-RH, respectively, were carried out on each subject at 8 am; the interval between tests was one week. The serum levels of LH and FSH were determined by radioimmunoassay (double-antibody method) before each injection, and 60, 120, 180, and 240 minutes after each injection. No differences in the basal values of either hormone were observed. In both oligospermic and normal men, maximal responses were obtained with doses between 100 and 250 mug. With 500 mug, levels decreased rather than increased. Maximal peaks occurred between 60 and 180 minutes after injection. In the two normal subjects, the responses of LH and FSH were similar. Two of the three oligospermic patients showed discordant responses. From the results, we can assume that LH-RH doses between 100 and 250 mug should be used as a basis for chronic treatment.

Adult↗
PubMed1979

Sleep-wake patterns and integrated values of luteinizing hormone, follicle stimulating hormone, prolactin, growth hormone and thyroid stimulating hormone in normal and cryptorchid pubertal patients.

The sleep-wake behaviour of LH, FSH, PRI, GH and TSH was studied in seven cryptorchid patients (four unilateral and three bilateral cryptorchids) average age 12 years and in nine normal pubertal boys of 13 years (mean age). Blood samples were collected by a continuous withdrawal pump, every hour, for 24 h. The hormonal concentration for every fraction of time was measured and related to the sleep (Sc-), wake (Wc-) and total 24 h period (Dc-). The integrated concentrations of the corresponding periods (IS, IW, ID) were calculated as well as their ratios (IS/IW; IS/ID%). For GH and TSH, the data obtained demonstrated no differences between cryptorchid and pubertal subjects. The PRL secretion in cryptorchid patients was moderately increased during the hours of nocturnal sleep. A normal pubertal sleep-wake rhythm was found for gonadotrophins in both groups of subjects. More marked levels of LH secretion were observed in cryptorchid boys compared to normal pubertals. The presence of a sleep-wake rhythm was also found in the cryptorchid patients and normal pubertal subjects in the P 1 stage. These data suggest that the CNS "programme" which controls the onset of puberty may be normal in cryptorchid patients.

Adolescent↗
PubMed1987

The higher the growth hormone response to growth hormone releasing hormone the lower the response to bromocriptine and thyrotrophin releasing hormone in acromegaly.

In acromegaly a direct relationship has been demonstrated between GH responsiveness to TRH and to the dopaminergic agent bromocriptine (Br). Recent data show an inverse relationship between GH responsiveness to Br and to GH releasing hormone (GHRH), but not between the GH responses to GHRH and TRH. Thirty-one acromegalic patients, 18 women and 13 men (age 46.2 +/- (SD) 13 years) were studied. Four patients had been treated, but all still had active disease. The GH responses to GHRH (hpGHRH1-44, Bachem 100 micrograms i.v. bolus), TRH (Thyroliberin, Hoechst 200 micrograms i.v. bolus) and Br (Parlodel 5 mg orally) were assessed in most of the patients. The GH responses to GHRH showed a wide interindividual variation (delta GH 1-995 ng/ml), which correlated significantly with the basal GH levels (r = +0.85, P less than 0.0001, n = 31). GH increments in response to GHRH were inversely related to the responses to Br, i.e. the lower the GH increase after GHRH the greater the GH decrease after Br (r = -0.49, P less than 0.01, n = 30). This decrease correlated with the basal PRL level (r = +0.45, P less than 0.02, n = 29) and also the GH response to TRH (r = +0.66, P less than 0.0001, n = 30). An inverse correlation was also found between the GH responses to TRH and to GHRH (r = -0.43, P less than 0.02, n = 29). The data are consistent with the existence of GH-secreting adenomas which are more sensitive to GHRH and less to Br and TRH (pure somatotroph adenomas) and of mixed (lactotroph-like adenomas) responsive to TRH and Br but less responsive to GHRH.

Acromegaly↗
PubMed1978

Effect of luteinizing hormone-releasing hormone on the secretion of luteinizing hormone, follicle-stimulating hormone, and testosterone in adult male rhesus monkeys.

Plasma levels of radioimmunoreactive LH, FSH, and testosterone (T) were assayed before and after administration of synthetic gonadotropin-releasing hormone (GnRH) to five chair-restrained rhesus monkeys with chronic indwelling venous catheters. Intravenous injection of 1, 5, and 25 microgram or infusion of 1 microgram/min for 25 min of GnRH resulted in a significant increase in plasma levels of LH. However, no significant increases in plasma FSH levels were detected. Plasma levels of T were also elevated after administration of 25 microgram GnRH, but peak concentration of T lagged behind peak levels of LH by approximately 30 min. These studies indicate that the male rhesus responds to GnRH administration by increased secretion of LH, followed by an increase in T levels. A concomitant increase in plasma FSH was not observed after treatment with GnRH in the doses used.

Animals↗
PubMed1994

Cytochemical detection of gonadotropin-releasing hormone-binding sites on rat pituitary cells with luteinizing hormone, follicle-stimulating hormone, and growth hormone antigens during diestrous up-regulation.

Pituitary cells with GnRH receptors increase over 2-fold during diestrus to reach a peak during the morning of proestrus. This is followed by a rapid fall during the afternoon of proestrus to reach a nadir by estrus. The objective of this study was to learn the identity of the new target cells added during diestrus. This was particularly important in view of recent evidence showing that gonadotropes with LH beta and FSH beta mRNA have GH antigens. Pituitary cells from diestrous and proestrous rats were exposed to biotinylated GnRH (Bio-GnRH) for 10 min. Bio-GnRH was detected by avidin peroxidase, and then the cells were immunolabeled for pituitary hormones. The percentages of cells labeled for Bio-GnRH rose during diestrus from 6.6 +/- 0.8% in the morning to 11.9 +/- 0.7% by evening (mean +/- SD). By the morning of proestrus, the percentages of Bio-GnRH target cells increased further to 16 +/- 0.7%. The percentages of pituitary cells dual labeled for LH beta antigens and Bio-GnRH rose from 4.3 +/- 0.6% to 9% +/- 1% during diestrus and averaged 13 +/- 0.7% by the morning of proestrus. At this time, 90% of cells with LH antigens bound Bio-GnRH. When percentages of pituitary cells with FSH beta antigens and Bio-GnRH-binding sites were analyzed, there was an increase during diestrus from 4 +/- 0.4% to 9.7 +/- 0.7%; a peak level of 14 +/- 0.9% was reached by the morning of proestrus. Bio-GnRH binding was expressed by 86% of FSH cells during this peak. Finally, GH antigens were also detected in GnRH target cells. The percentage of cells dual labeled for Bio-GnRH and GH increased from 4 +/- 0.8% to 8 +/- 1% during diestrus and the morning of proestrus. During the diestrous and proestrous peak periods of expression, Bio-GnRH binding was seen in 32% of GH cells. None of the other pituitary cell types showed significant GnRH binding. These studies showed that most of the new GnRH-receptive cells stem from maturing gonadotropes. Half of the GnRH-receptive cells also contain GH antigens, which correlated with results from previous studies that showed GH antigens in cells with gonadotropin mRNAs. This might reflect expression of gonadotrope functions by a subset of GH cells. Alternatively, the GH antigens may be bound to GH receptors in gonadotropes. This latter possibility may signify a paracrine regulation of gonadotrope function by GH.

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↗
PubMed1989

Effect of intranasal growth hormone-releasing hormone and corticotropin-releasing hormone administration on growth hormone and cortisol release: improved bioavailability by means of sodium-glycocholate.

Several peptide hormones are effective when administered intranasally (in); these include oxytocin, vasopressin, insulin, glucagon, and calcitonin. With regard to GHRH and CRH, previous studies demonstrated that their bioavailability following in administration was very low. In this study we evaluated the serum GH response to 50 micrograms GHRH iv and to 700 micrograms GHRH in, the latter given alone and with 5 and 15 mg sodium-glycocholate (SGC), a surfactant, in six normal men. The bioavailability of in GHRH, calculated as net GH secretory area, was very low, and increased to 7% that of iv GHRH when SGC was used. In the same men, 50 micrograms CRH was administered both iv and in, alone and with 5 and 15 mg SGC. The bioavailability of in CRH, calculated as net cortisol secretory area, was very low and increased to 100% that of iv CRH when 15 mg SGC was used. These data indicate that the efficacy of GHRH and CRH administered in is significantly augmented by SGC.

Administration, Intranasal↗