The roles of hypothalamic growth hormone-releasing hormone (GHRH) and of somatostatin (SRIF) in pharmacologically stimulated growth hormone (GH) secretion in humans are unclear. GH responses could result either from GHRH release or from acute decline in SRIF secretion. To assess directly the role of endogenous GHRH in human GH secretion, we have used a competitive GHRH antagonist, (N-Ac-Tyr1,D-Arg2)GHRH(1-29)NH2 (GHRH-Ant), which we have previously shown is able to block the GH response to GHRH. We first tested whether an acute decline in SRIF, independent of GHRH action, would release GH. Pretreatment with GHRH-Ant abolished the GH response to exogenous GHRH (0.33 microgram/kg i.v.) but did not modify the GH rise after termination of an SRIF infusion. We then investigated the role of endogenous GHRH in the GH responses to pharmacologic stimuli of GH release. The GH responses to arginine (30 g i.v. over 30 min), L-dopa (0.5 g orally), insulin hypoglycemia (0.1 U/Kg i.v.), clonidine (0.25 mg orally), or pyridostigmine (60 mg orally) were measured in healthy young men after pretreatment with either saline of GHRH-Ant 400 microgram/kg i.v. In every case, GH release was significantly suppressed by GHRH-Ant. We conclude that endogenous GHRH is required for the GH response to each of these pharmacologic stimuli. Acute release of hypothalamic GHRH may be a common mechanism by which these compounds mediate GH secretion.

/pdf/endogenous-growth-hormone-gh-releasing-hormone-is-required-4s5k5646du.pdf

Endogenous growth hormone (GH)-releasing hormone is required for GH responses to pharmacological stimuli.

Objective: The role of endogenous GHRH in arginine-, insulin-, clonidine- and L-dopa-induced GH secretion was studied in man using a GHRH antagonist (GHRH-Ant). Design: Ten healthy adult males were studied for serum GH responses to arginine or insulin singly, or sequentially 120 min after GHRH injection with or without combined administration of GHRH-Ant. Further, GHRH, clonidine or L-dopa were sequentially administered to these subjects 120 min after the GHRH injection. Results: The combined administration of GHRH-Ant distinctly inhibited the arginine- and insulininduced GH release. When these four agents were sequentially administered 120 min after GHRH injection, the GH responses to clonidine and L-dopa disappeared completely while clear responses were observed to arginine and insulin administration. These responses to arginine and insulin were also completely inhibited by the combined administration of GHRH-Ant. Conclusions: These results indicate that clonidine and L-dopa stimulate GH secretion mainly through the release of hypothalamic GHRH, and that arginine- and insulin-induced hypoglycaemia stimulate GH secretion mainly through the inhibition of hypothalamic somatostatin release. However, the presence of endogenous hypothalamic GHRH seems to be essential for the maximal stimulation of GH release induced by arginine and insulin.

/pdf/the-role-of-endogenous-ghrh-in-arginine-insulin-clonidine-37q5mnld2e.pdf

The role of endogenous GHRH in arginine-, insulin-, clonidine- and l-dopa-induced GH release in normal subjects.

Background. Previous studies have suggested that the neuroendocrine control of growth hormone (GH) secretion changes with increasing age in women with normal menstrual cycles and sex steroid levels. Methods. In order to verify this hypothesis, 8 younger (22-32 years) and 8 older (41-45 years) women with normal menstrual function and gonadal steroid levels were tested with the serotonergic agent sumatriptan (6 mg in a subcutaneous bolus), the GABAergic agonist sodium valproate (800 mg orally), the dopaminergic compound L-Dopa (500 mg orally) and placebos. Furthermore, all women were tested with GH-releasing hormone (GH-RH 1 pg/kg body weight in an intravenous (i.v.) bolus) to determine whether GH secretion in response to its specific releasing factor was preserved. Serum GH levels were recorded over 2 hours in all tests and IGF-I levels in basal samples. Results. Plasma IGF-I concentrations and the GH responses to sumatriptan, sodium valproate and L-Dopa were significantly lower in older than in younger women. Also, the GH-RH-induced GH response was significantly lower in older than in younger subjects. When peak GH responses to releasing stimuli were compared with age, significant negative correlations were found in all tests. Conclusions. These data did not show a specific neurotransmitter change underlying defective GH secretion in older aged reproductive women. On the other hand, the results indicated that age-related changes in the secretory machinery of GH, such as a reduced pituitary sensitivity to GH-RH and/or a reduction in the pituitary GH secretory capacity, affect women during the last years of the reproductive period.

/pdf/altered-neuroendocrine-control-of-gh-secretion-in-normal-axk0tcjrut.pdf

Altered Neuroendocrine Control of GH Secretion in Normal Women of Advanced Reproductive Age

GH secretion status in myotonic dystrophy

To determine how L-dopa stimulates GH secretion, we investigated its interaction with GHRH in vivo. Six normal men were studied on 4 occasions: 1) L-dopa-TRH: 500 mg L-dopa orally followed by 200 µg TRH 60 min later; 2) L-dopa-GHRH-TRH: 100 µg GHRH 1-44 iv 30 min after L-dopa followed by 200 µg TRH iv; 3) GHRH-TRH: 100 µg GHRH iv at 0 min, 30 min later 200 µg TRH iv; 4) TRH test: 200 µg TRH iv as a bolus. After L-dopa-TRH GH-levels increased significantly from 0.6 µg/l to 25.8 ± 9.6 (SE) µg/l at 60 min. Only a slight TSH and no PRL increase was observed after L-dopa-TRH. After L-dopa-GHRH-TRH the GH-increase was significantly higher (45.7 ± 11.1 µg/l) compared to L-dopa-TRH alone. GHRH-TRH increased GH-levels to 52.5 ± 12.1 µg/l, which was not significantly different from the GH-levels obtained when L-dopa-GHRH-TRH were given. TRH increased serum TSH and PRL to 6.3 ± 0.7 µU/ml and 715 ± 136 µU/ml, respectively, which was significantly higher compared to the TSH responses after L-dopa-TRH. The PRL and TSH increase after TRH only was also higher (TSH-max: 5.7 ± 0.5 µU/ml; PRL-max: 899 ± 154 µU/ml) compared to the TSH and PRL responses after L-dopa-TRH. Our results show that the combination of L-dopa with GHRH leads to the same GH response as GHRH only. However, both responses are significantly higher than the one after L-dopa alone. This observation indicates that the stimulatory effect of L-dopa on GH secretion is mediated by endogenous GHRH. The inhibition of the TSH and PRL response to TRH after L-dopa administration, however, is due to the direct action of the L-dopa metabolite dopamine on the anterior pituitary.

Interaction of L-dopa and GHRH on GH secretion in normal men

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Interaction of L-dopa and GHRH on GH secretion in normal men