Acetylcholine Inhibits the Release of Somatostatin from Rat Hypothalamus in Vitro*

Richardson, Stephen B.; Hollander, Charles S.; D'eletto, Richard D.; Greenleaf, Peter; Thaw, Colette N.

doi:10.1210/endo-107-1-122

Cited by 173 publications

(79 citation statements)

References 43 publications

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“…The present understanding of their effects has been based upon in vitro studies of hypothalamic and pituitary tissues, indirect animal and human studies, and direct measurement of hypothalamic GHRH and SRIF output in animals. A suprapituitary site of action of these stimuli is exemplified by the lack of GH responses in animals that have undergone hypothalamic ablation (16) and in humans with hypothalamic lesions (17), by the inability of these stimuli to release GH from isolated pituitaries (18), and by the modulation of GHRH and/or SRIF release in vitro (19) and in vivo (20, 21) during pharmacologic stimulation.…”

Section: Discussionmentioning

confidence: 99%

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

1996

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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-Tyr 1 , D -Arg 2 )GHRH(1-29)NH 2 (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 g/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 or GHRHAnt 400 g/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. ( J. Clin. Invest. 1996. 97: 934-940.)

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Section: Discussionmentioning

confidence: 99%

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

1996

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“…In that respect, ARG has been shown to override inhibitory effects on GH secretion that are known to be mediated by an increase in somatostatin release, including glucose administration (Ghigo et al, 1992), obesity Martina et al, 1995), glucocorticoids (Giustina et al, 1992), advanced age (Ghigo et al, 1990b) and GH negative feedback (Massara et al, 1986;Torsello et al, 1988;Kelijman and Frohman, 1991;Ghigo et al, 1991). Cholinesterase inhibitors, such as neostigmine (NEO) and pyridostigmine, which are known to decrease somatostatin release (Richardson et al, 1980;Muller, 1987) do not further increase GH response to ARG in human (Massara et al, 1986;Ghigo et al, 1990aGhigo et al, , 1994Procopio et al, 1995). On the contrary, the effect of ARG on GH secretion is blunted or abolished by cholinergic antagonists such as atropine (Casanueva et al, 1984) and pirenzepine (Delitala et al, 1982;Maccario et al, 1995), an acute increase in free fatty acids (Maccario et al, 1994) and an administration of a somatostatin analog (Masuda et al, 1990).…”

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confidence: 99%

Effects of arginine, growth hormone-releasing hormone (GHRH) and neostigmine administered singly or in paired combinations on growth hormone (GH) release in pigs

Cochard¹,

Guilhermet²,

Bonneau³

1997

Reprod. Nutr. Dev.

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Summary -In human, arginine (ARG) induces growth hormone (GH) release, probably via a decrease in somatostatinergic tone. To assess the mechanism by which ARG mediates GH release in pigs, the effects on plasma GH release of ARG ( 1 g/kg body weight, infused between times -15 and -5 min), growth hormone-releasing hormone (GHRH, 2 pg/kg, at time 0 min) and neostigmine, a cholinesterase inhibitor (NEO, 50 arginine / growth hormone-releasing hormone / néostigmine / hormone de croissance / porc

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“…The release of the hypothalamic peptides is in turn influenced by various neurotransmitters, for example cholinergic agonists increase and antagonists decrease GH release (2,3). Data in animals suggest that the effects of altered cholinergic tone are mcdiated through alterations in hypothalamic somatostatin secretion (4,5). Pyridostigmine, an acetylcholinesterase inhibitor, augments cholinergic tone, and increases both basal and GHRHstimulated GH release (6, 7).…”

mentioning

confidence: 99%

Pyridostigmine, an Acetylcholinesterase Inhibitor, Stimulates Growth Hormone Release, but has no Effect on Basal Thyrotrophin or Adrenocorticotrophin Levels, or the Thyrotrophin Response to Thyrotrophin‐Releasing Hormone

Freeman

Touzel

Grossman

et al. 1990

J Neuroendocrinology

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Pyridostigmine, an acetylcholinesterase inhibitor, stimulates growth hormone (GH) release and is thought to act by inhibiting hypothalamic somatostatin release. There are few data concerning the effect of pyridostigmine on other pituitary hormones apart from GH. We have studied the effect of pyridostigmine on basal GH, thyrotrophin (TSH), prolactin, adrenocorticotrophin and cortisol release, and thyrotrophin-releasing hormone (TRH)-stimulated TSH and prolactin release, in two studies involving nine healthy male subjects. Pyridostigmine stimulated GH release in all subjects but had no effect on adrenocortocotrophin or cortisol levels, or basal or TRH-stimulated TSH and prolactin levels.There are some data to suggest that somatostatin inhibits TRH-stimulated TSH release. Our findings, however, suggest that either endogenous somatostatin tone has little effect on the TSH response to TRH compared to its effects on GH or pyridostigmine acts through a mechanism other than altering somatostatin tone. Pyridostigmine did not alter adrenocorticotrophin or cortisol levels in the presence of a clear action on GH release, providing further evidence that the previously reported effects of cholinergic drugs on cortisol release are stress-relatedThe pulsatile release of growth hormone (GH) results from a d! namic equilibrium between the two hypothalamic hormones, Somatostatin and GH-releasing hormone (GHRH) (1). They act rehpectively to inhibit and stimulate GH release from the pituitary. The release of the hypothalamic peptides is in turn influenced by various neurotransmitters, for example cholinergic agonists increase and antagonists decrease GH release (2, 3). Data in animals suggest that the effects of altered cholinergic tone are mcdiated through alterations in hypothalamic somatostatin secretion (4, 5). Pyridostigmine, an acetylcholinesterase inhibitor, augments cholinergic tone, and increases both basal and GHRHstimulated GH release (6, 7). To date, there are few data concerning the effect of altered cholinergic tone on the release of other pituitary hormones. Exogenous somatostatin inhibits the thyrotrophin (TSH) response to thyrotrophin-releasing hormone (TKH) (8,9), and therefore it might be expected that alterations in cholinergic tone could influence TSH release. In vitro, acetylcholine causes release of corticotrophin-releasing factor (10, 11) but its effects in vivo remain unclear (12). We have therefore studied the effect of pyridostigmine on basal GH, TSH, prolactin and adrenocorticotrophin (ACTH) release, and the TSH, GH and prolactin responses to TRH. Results Study IIn all six subjects GH levels rose 60 to 120 min after pyridostigmine and were higher than after placebo alone. After 60 min the mean peak serum GH level after placebo was 3.8 (range, < 1.0 to 9.0) mU/1 compared to 23.0 (5.5 to 52.6) mU/1 after pyridostigmine (P=O.O36). There was no consistent change in either ACTH or cortisol levels after pyridostigmine as compared to placebo (Fig. I), but in one subject ACTH levels rose from 13 ng/l at t...

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Acetylcholine Inhibits the Release of Somatostatin from Rat Hypothalamus in Vitro*

Cited by 173 publications

References 43 publications

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

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

Effects of arginine, growth hormone-releasing hormone (GHRH) and neostigmine administered singly or in paired combinations on growth hormone (GH) release in pigs

Pyridostigmine, an Acetylcholinesterase Inhibitor, Stimulates Growth Hormone Release, but has no Effect on Basal Thyrotrophin or Adrenocorticotrophin Levels, or the Thyrotrophin Response to Thyrotrophin‐Releasing Hormone

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