Inhibitory Effect of Antimuscarinic Cholinergic Drug (Atropine) on Growth Hormone (GH) Secretion Induced by GH-Releasing Factor

Yagi, Hirofumi; Nagashima, Kei; Noji, Tohru; Yunoki, Hitosi; Suzuki, Shunsuke; Kuroume, Takayosi

doi:10.1055/s-2007-1012419

Cited by 3 publications

(1 citation statement)

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“…That the hy¬ pothalamic component of Sm-C negative feedback on GH secretion may be mediated by SRIH is sup¬ ported by the ability of Sm-C to induce an in¬ creased SRIH release from rat hypothalami in vitro (Berelowitz et al 1981). Consistent with this view is also the increased release of SRIH from the hypothatami of rats with spontaneous experimen¬ tal obesity (Berelowitz et al 1983). Recently, data have been presented showing that cholinergic muscarinic agonists or antagonistic drugs modulate in an opposite way the GH rise elicited by GHRH (Massara et al 1984(Massara et al , 1986aCasanueva et al 1986;Yagi et al 1986), likely via a somatostatinergic mechanism (Richardson et al 1980;Locatelli et al 1986). …”

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Pyridostigmine counteracts the blunted growth hormone response to growth hormone-releasing hormone of obese children

Loche

Pintor

Cappa³

et al. 1989

Acta Endocrinologica

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We have evaluated the effect of acute administration of pyridostigmine bromide, a cholinesterase inhibitor, on the GHRH-induced GH rise in 11 obese children and in 8 age-matched controls. The GH response to GHRH (hpGRF 1\p=n-\40, 1 \g=m\g/kg iv), evaluated both as maximum GH peak and as integrated area under the curve, was significantly lower in the obese children than in the controls. Pretreatment with pyridostigmine bromide (60 mg orally 60 min before the GHRH injection) significantly increased both baseline GH levels and the GH response to GHRH in all the obese subjects, so that their mean baseline GH, peak GH levels and integrated area under the curve after pyridostigmine bromide plus GHRH were similar to those of the control children after GHRH. Also in control children pyridostigmine bromide increased (though not significantly) baseline GH levels, and caused a significant augmentation of the GH response to GHRH. Mean peak GH levels and mean integrated area under the curve after pyridostigmine bromide plus GHRH were significantly higher in the controls than in the obese children given the same treatment. Mean baseline Sm-C levels were significantly higher in the obese than in control children. These data show that enhancement of cholinergic neurotransmission, likely in the hypothalamus, counteracts the blunted GH response to GHRH present in the obese children, and that in simple obesity the potential of the pituitary to make a secretory response to a direct GH secretagogue is preserved.

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confidence: 99%

Pyridostigmine counteracts the blunted growth hormone response to growth hormone-releasing hormone of obese children

Loche

Pintor

Cappa³

et al. 1989

Acta Endocrinologica

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Peptide and Protein Hormones

König

2000

Ullmann's Encyclopedia of Industrial Chemistry

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Pyridostigmine-mediated growth hormone release: evidence for somatostatin involvement.

et al. 1992

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Pyridostigmine (PD), a cholinesterase inhibitor, has been shown to elicit GH release when given alone and to potentiate the GH response to GH-releasing hormone (GHRH) in man. Numerous experiments have indirectly indicated that somatostatin (SS) inhibition is its likely mechanism of action. This study sought to establish the ability of PD to induce GH release in the rat, determine the dose-response relationship, and test the hypothesis that SS inhibition is the method of action. Three experiments were performed to monitor the GH response to PD. I) Five groups of male rats were food deprived for 72 h. The groups were then treated iv with saline, SS antibody (SS-ab), and 10, 100, and 1000 micrograms/kg PD, respectively. Blood samples were drawn before and after treatment. II) Two groups of male rats were pretreated iv with GHRH antibody (GHRH-ab) and either SS-ab or normal sheep serum (NSS). Blood samples were drawn every 30 min for 8.5 h, during which time each animal was injected with PD (10 micrograms/kg) in the third hour and again in the sixth hour. III) Male rats received a PD injection (10 micrograms/kg, iv) during a spontaneous GH trough period and a second PD injection during a spontaneous GH peak period. Blood samples were drawn at regular intervals preceding and following treatments. In Exp I, PD induced a clear 4- to 5-fold increase in GH concentrations in food-deprived rats. The maximal GH responses occurred after the 10 and 100 micrograms/kg doses, although the pattern and duration were different with these two doses. In Exp II, PD induced an approximately 2-fold increase in GH values in animals pretreated with GHRH-ab and NSS, but failed to induce a change in GH in the animals treated with GHRH-ab and SS-ab. In Exp III, PD failed to induce any change in GH concentration when administered during spontaneous GH peaks or troughs. The first two experiments suggest that PD increases GH secretion in the rat via inhibition of SS. The failure of PD to alter GH during a spontaneous peak is consistent with the current hypothesis that the level of SS is low at this time. Its failure to alter GH during trough periods may be related to very high SS tone. In conclusion, our results support the hypothesis that PD acts via inhibition of SS secretion.

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Inhibitory Effect of Antimuscarinic Cholinergic Drug (Atropine) on Growth Hormone (GH) Secretion Induced by GH-Releasing Factor

Cited by 3 publications

References 5 publications

Pyridostigmine counteracts the blunted growth hormone response to growth hormone-releasing hormone of obese children

Pyridostigmine counteracts the blunted growth hormone response to growth hormone-releasing hormone of obese children

Peptide and Protein Hormones

Pyridostigmine-mediated growth hormone release: evidence for somatostatin involvement.

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