Inhibition by Somatostatin on the Release of TSH Induced in Man by Thyrotropin-Releasing Factor

Siler, T.M.; Yen, S. S. C.; Vale, Wylie; Guillemin, Roger

doi:10.1210/jcem-38-5-742

Cited by 236 publications

(62 citation statements)

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“…Acetylcholine inhibits somatostatin release from the rat hypothalamus (4), and the effects of cholinergic manipulation on GH secretion in rats was abolished by hypothalamic somatostatin depletion (5). Somatostatin given as an infusion in man inhibits the TSH response to TRH (8,9), while in the rat antiserum to somatostatin increases basal TSH release and the TSH response to cold (15). This evidence that somatostatin has a physiological role inhibiting TSH release has frequently been cited when interpreting studies of GH secretion.…”

Section: Discussionmentioning

confidence: 99%

“…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).…”

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confidence: 99%

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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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Section: Discussionmentioning

confidence: 99%

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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“…The name SST originates from a supposed 'specific' function as an inhibitor of somatotropin (growth hormone (GH)) release, thus somatotropin release-inhibiting factor. In the CNS, SST has a key inhibitory action in the secretion of GH (Brazeau et al 1973), prolactin (PRL; Vale et al 1974), thyrotropin (Siler et al 1974), and ACTH (Richardson & Schonbrunn 1981, Lamberts et al 1989a from the anterior pituitary gland. At the peripheral nervous system level, SST plays a regulatory role in the gastrointestinal tract inhibiting flow from the gallbladder, bowel motility and gastric emptying, smooth muscle contraction, and nutrient absorption from the intestine as well as in the exocrine pancreas.…”

Section: Somatostatin Receptor Ligandsmentioning

confidence: 99%

Treatment of Cushing's disease: a mechanistic update

Cuevas‐Ramos¹,

Fleseriu²

2014

Journal of Endocrinology

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Cushing's disease (CD) is characterized by an ACTH-producing anterior corticotrope pituitary adenoma. If hypothalamus-pituitary-adrenal (HPA) axis physiology is disrupted, ACTH secretion increases, which in turn stimulates adrenocortical steroidogenesis and cortisol production. Medical treatment plays an important role for patients with persistent disease after surgery, for those in whom surgery is not feasible, or while awaiting effects of radiation. Multiple drugs, with different mechanisms of action and variable efficacy and tolerability for controlling the deleterious effects of chronic glucocorticoid excess, are available. The molecular basis and clinical data for centrally acting drugs, adrenal steroidogenesis inhibitors, and glucocorticoid receptor antagonists are reviewed, as are potential novel molecules and future possible targets for CD treatment. Although progress has been made in the understanding of specific corticotrope adenoma receptor physiology and recent clinical studies have detected improved effects with a combined medical therapy approach, there is a clear need for a more efficacious and better-tolerated medical therapy for patients with CD. A better understanding of the molecular mechanisms in CD and of HPA axis physiology should advance the development of new drugs in the future.

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“…The fact that in group I (• •, n=32) and group II the postinhibitory GH rise after somatostatin infusion was much smaller in group II than in group I suggests the following possibilities, 1) intracellularly stored GH pool was smaller in these patients due to lesser GH inhibition, 2) negative feedback effects on their hypothalamic GHRH or somatostatin were less prominent, or 3) these somatotrophs were less responsive to endogenous hypothalamic stimulations through such feedback (Hanew et al 1984). From the data of similar plasma TSH responses to TRH in the two groups, it seems that negative feedback effects of OH on hypothalamic somatostatin secretion are essentially not different in the two groups, since it is well known that somatostatin can regulate TSH secretion in man and rat (Siler et al 1974;Chihara et al 1978 (Shibasaki et al 1986). Relating to this, the receptor site of GHRH and somatostatin, using the pituitary adenomas in vitro, are reported to be different (Lamberts et al 1984).…”

Section: Discussionmentioning

confidence: 89%

The spectrum of GH responses to GHRH and somatostatin in patients with acromegaly.

Hanew

Sato

Goh

et al. 1988

Tohoku J. Exp. Med.

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Inhibition by Somatostatin on the Release of TSH Induced in Man by Thyrotropin-Releasing Factor

Cited by 236 publications

References 0 publications

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

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

Treatment of Cushing's disease: a mechanistic update

The spectrum of GH responses to GHRH and somatostatin in patients with acromegaly.

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