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PubMedDate not supplied

Effects of the gonadotropin-releasing hormone associated peptides (GAP) on the release of luteinizing hormone (LH), follicle stimulating hormone (FSH) and prolactin (PRL) in vivo.

Six peptide sequences residing between basic amino acid residues in GAP were tested for effects on the release of FSH, LH and PRL in vivo in ovariectomized, estrogen-progesterone-primed (OEP) rats. Synthetic GAP peptides (1-13, 1-23, 15-23, 25-36, 38-53 and 41-53) were injected intravenously (IV) into conscious OEP rats and plasma levels of FSH, LH and PRL were measured by RIA. The activity of GAP peptides in the control of PRL was further examined in ether-stressed male rats which were injected IV with GAP peptides just prior to a 1-min etherization. GAP(1-13) significantly stimulated FSH release at doses of 1, 10 and 100 micrograms, whereas it stimulated LH release only at the highest dose of 100 micrograms. GAP(1-23) elevated plasma levels of FSH and LH only at a dose of 100 micrograms. The other 4 peptides had no effect on the release of gonadotropins. Of these 6 peptides, only GAP(1-13) partially lowered the plasma levels of PRL at the high dose of 100 micrograms in OEP rats, but it had no effect on the ether-induced PRL surge at doses of 10 and 100 micrograms. In conclusion, both GAP(1-13) and GAP(1-23) stimulate FSH and LH release in vivo; these 2 peptides are much less potent in stimulating gonadotropin release than is LHRH. GAP(1-13) exerts a preferential FSH-releasing activity, but its PRL-inhibiting activity is minimal.

Animals↗
PubMed1993

Growth hormone response to growth hormone-releasing hormone in early abstinent alcoholic patients.

The alpha-2-adrenoceptor agonist clonidine is able to stimulate GHRH secretion directly or via beta-endorphin and, therefore, induces a GH release in normal subjects. This effect has been shown to be blunted in alcoholism during early abstinence, due to central alterations of adrenergic mechanisms. To evaluate pituitary responsiveness to direct stimulation with GHRH, we have studied the GH and PRL response to GHRH in 10 alcoholics during early abstinence. Our data indicate that the pituitary response to GHRH is intact in abstinent alcoholics, except in obese patients, who displayed a blunted GH response. GHRH did not increase PRL. The dissociation between clonidine and GHRH in GH stimulation could reveal a different neuroendocrine mechanism, in comparison with other psychiatric disorders (anorexia nervosa), in which such a dissociation is accompanied by a PRL response to GHRH.

Adult↗
PubMed2005

Serum luteinizing hormone in patients undergoing ovarian stimulation with gonadotropin-releasing hormone antagonists and recombinant follicle-stimulating hormone and its relationship with cycle outcome.

The serum LH was determined on days 3, 6, and 8 of stimulation and on the day of hCG in 110 normogonadotropic patients undergoing controlled ovarian hyperstimulation (COH) for IVF induced with GnRH antagonists and recombinant FSH, creating three groups of patients according to Tukey's hinges (percentiles 25 and 75) for each determination. No differences were observed between the number of oocytes recovered or the fertilization, implantation, and pregnancy rates (PR) of the groups, although patients with high serum LH levels during stimulation showed significantly higher serum E2 levels on the day of hCG.

Adolescent↗
PubMed2000

The effects of a continuous infusion of hexarelin on pulsatile growth hormone release, growth axis and galanin gene expression and on the response of the growth axis to growth hormone-releasing hormone.

The effect of a 6 hour continuous infusion of Hexarelin (100 micrograms/hour) on GH peak frequency, amplitude and duration, GH trough concentrations, the interval between successive peaks and the pituitary responsiveness to GHRH, as well as GH axis and galanin mRNA contents, were examined in conscious adult male rats. Plasma GH concentrations peaked within 15 minutes after the initiation of Hexarelin infusion, but returned to baseline levels by 60 minutes. No significant differences between Hexarelin and saline infused rats were noted for any of the parameters of pulsatile GH release analyzed. However, following a 6 hour infusion, rats treated with Hexarelin demonstrated a greater GH responsiveness to GHRH (delta GH: 57 +/- 16 ng/ml for Hexarelin infused; 21 +/- 7 ng/ml for saline infused; p < 0.05). Furthermore, the rats infused with Hexarelin demonstrated decreased GHRH and increased hypothalamic galanin mRNA contents as compared to the saline infused rats, while hypothalamic somatostatin and pituitary GH mRNA contents appeared unchanged. Rats infused with Hexarelin had lower pituitary galanin mRNA content than did the rats which were infused with saline. Collectively, these results suggest that Hexarelin may not act via alteration of somatostatin synthesis and that suppression of somatostatin's action at the pituitary can not be excluded. The current study also suggests that other hypothalamic pathways aside from those currently defined for the growth axis may be involved in the mechanism by which Hexarelin and the other GH-releasing peptides elicit GH release.

Animals↗
PubMed1988

The influence of age on human pancreatic growth hormone releasing hormone stimulated growth hormone secretion.

63 non-obese healthy subjects aged 18 to 95 years were investigated for age-dependence of GHRH-stimulated GH-secretion. In addition, priming of GH-secretion with three oral doses of propranolol (3 x 80 mg, the last dose 2 hours prior to the second GHRH-bolus) was carried out in 15 subjects below 40 years and 13 subjects older than 70 years. We found that mean maximal incremental GH-levels were inversely correlated with chronological age (r = -0.44, P = 0.001) of the probands. Propranolol premedication caused a significant rise of both basal and peak GHRH-induced relative increases in all subjects tested, whereas GHRH-induced relative increases of GH remained unchanged. In a well selected group of non-obese healthy subjects stimulated GH-secretion is found to undergo an aging process that is supposed to be of pituitary and suprapituitary origin. Priming GH-secretion with a beta-Blocker is possible both in young and very old healthy subjects and is likely to affect the basal GH secretory tone and not GHRH-stimulated GH-secretion.

Adult↗
PubMed1995

Adrenergic and cholinergic involvement in basal and growth hormone-releasing hormone-stimulated growth hormone secretion in glucocorticoid-treated rats.

Glucocorticoids are known to inhibit GH secretion via somatostatin. The aim of our study was to elucidate the involvement of somatostatin in the GH-releasing action of the alpha 2 agonist clonidine and the cholinergic agent pyridostigmine in conscious, freely-moving rats chronically treated with dexamethasone. After seven days of chronic glucocorticoid treatment, animals received an i.v. injection of either saline (1 ml/kg) or clonidine (150 micrograms/kg) or pyridostigmine (100 micrograms/kg) at -15 min. Three blood samples were then drawn (-10 min, -5 min, and 0 min) to assess the GH response to either clonidine or pyridostigmine alone. After the 0 min sample, saline (1 ml/kg) or GNRH (500 ng/kg) was injected i.v. and additional blood samples were drawn from 5 to 30 min. The GH response to clonidine alone or combined with GNRH in rats treated with dexamethasone was significantly lower (p < 0.05) as compared to vehicle-treated rats. The GH response to pyridostigmine alone or combined with GNRH did not significantly differ between vehicle- and dexamethasone-treated rats. These data suggest that in the rat the mechanism of action of clonidine is mainly to stimulate endogenous GNRH secretion, while pyridostigmine appears to predominantly act by decreasing hypothalamic somatostatin.

Adrenergic alpha-Agonists↗