Opioid modulation of the gamma-aminobutyric acid-controlled inhibition of exercise-stimulated growth hormone and prolactin secretion in normal men

1994 ◽  
Vol 131 (1) ◽  
pp. 50-55 ◽  
Author(s):  
V Coiro ◽  
R Volpi ◽  
ML Maffei ◽  
A Caiazza ◽  
G Caffarri ◽  
...  

Coiro V, Volpi R, Maffei ML, Caiazza A, Caffarri G, Capretti L, Colla R, Chiodera P. Opioid modulation of the gamma-aminobutyric acid-controlled inhibition of exercise-stimulated growth hormone and prolactin secretion in normal men. Eur J Endocrinol 1994;131:50–5. ISSN 0804–4643 The possible involvement of endogenous opioids in the gamma-aminobutyric acid-controlled (GABAergic) inhibition of growth hormone (GH) and prolactin (PRL) during physical exercise was evaluated in normal men. After fasting overnight, seven subjects were tested on four mornings at least 1 week apart. Exercise was performed on a bicycle ergometer. The workload was gradually increased at 3-min intervals until exhaustion and lasted about 15 min in all subjects. Tests were carried out under administration of placebo, the opioid antagonist naloxone (10 mg as an iv bolus injection), the GABAergic agonist sodium valproate (600 mg in three divided doses orally) or naloxone plus sodium valproate. During exercise, plasma GH and PRL levels rose 5.5- and 1.9-fold, respectively. The administration of naloxone did not modify, whereas sodium valproate significantly reduced the plasma GH and PRL rise during exercise. In the presence of sodium valproate, GH and PRL levels rose 3- and 1.5-fold, respectively, in response to exercise. When naloxone was given together with sodium valproate, both GH and PRL responses to exercise were abolished completely. These data suggest the involvement of a GABAergic mechanism in the regulation of GH and PRL responses to physical exercise in men. Furthermore, the data argue against a role of naloxone-sensitive endogenous opioids in the control of these hormonal responses to exercise, whereas they suggest a modulation by opioids of the GABAergic inhibitory action. Vittorio Coiro, Istituto di Clinica Medica Generale e Terapia Medica, Università di Parma, via Gramsci 14, 43100 Parma, Italy

1988 ◽  
Vol 119 (3) ◽  
pp. 353-357 ◽  
Author(s):  
Palmiero Monteleone ◽  
Mario Maj ◽  
Michele Iovino ◽  
Luca Steardo

Abstract. Evidence has been provided supporting the existence of a sex-related difference in the GH secretion following different GH-releasing stimuli. Since pharmacological activation of the endogenous gamma-aminobutyric acid (GABA) system results in increased basal GH release in humans, the present study was undertaken to investigate whether a sex difference is present in the GH response to GABAergic stimulation. Sixteen healthy subjects (8 women and 8 men) received orally 10 mg of baclofen, the direct GABAB agonist which freely crosses the blood-brain barrier. Blood samples were collected before (T = −30 and 0) and 30, 60, 90, 120 and 180 min after the drug administration for plasma GH measurements. Following baclofen administration, plasma GH rose in healthy males (F = 19.417, P < 0.0001), but not in females (F = 1.67, NS). These results suggest that GABA modulation of human GH release is sex-dependent.


1977 ◽  
Vol 45 (3) ◽  
pp. 579-584 ◽  
Author(s):  
F. CAVAGNINI ◽  
C. INVITTI ◽  
A. DI LANDRO ◽  
L. TENCONI ◽  
C. MARASCHINI ◽  
...  

1980 ◽  
Vol 93 (2) ◽  
pp. 149-154 ◽  
Author(s):  
F. Cavagnini ◽  
C. Invitti ◽  
M. Pinto ◽  
C. Maraschini ◽  
A. Di Landro ◽  
...  

Abstract. A single oral dose of 5 g gamma aminobutyric acid (GABA) was given to 19 subjects and serial venous blood samples were obtained before and 3 h after drug administration. A placebo was administered to 18 subjects who served as controls. GABA caused a significant elevation of plasma growth hormone levels (P < 0.001), but did not consistently alter plasma prolactin concentration since only 5 out of 15 subjects showed an increase of the hormone. Eight additional subjects were submitted to an insulin tolerance test before and after per os administration of 18 g GABA daily for 4 days. Protracted GABA treatment significantly blunted the response of growth hormone and enhanced that of prolactin to insulin hypoglycaemia (P < 0.01). These results indicate that pharmacological doses of GABA affect growth hormone and prolactin secretion in man. The precise nature of GABA's effects as well as its mechanism of action remains to be clarified.


1990 ◽  
Vol 127 (3) ◽  
pp. 461-469 ◽  
Author(s):  
E. Ssewannyana ◽  
G. A. Lincoln

ABSTRACT In a group of adult Soay rams housed indoors under an artificial light cycle of alternating 16-week periods of long and short days, there was a conspicuous longterm cycle in the peripheral plasma concentrations of β-endorphin and prolactin. The levels of β-endorphin were highest under short days and lowest under long days (15-fold change), and inversely related to the changes in the plasma levels of prolactin (120-fold change). The role of dopamine in the control of β-endorphin and prolactin was investigated in a series of experiments, conducted under both long and short days, in which rams were treated with dopamine receptor agonists (dopamine and bromocriptine) and antagonists (pimozide and sulpiride). Naloxone (opioid antagonist) was also administered to assess the additional involvement of endogenous opioids. Dopamine injected i.v. (6·6 mg/kg every 10 min) did not significantly affect the mean plasma concentrations of β-endorphin and prolactin under either long or short days. Pimozide (0·08 mg/kg i.m. every 2 h) caused a large increase in the mean plasma concentrations of β-endorphin and prolactin under long days but not short days. Naloxone (1·6 mg/kg, i.v.), administered alone or in combination with dopamine or pimozide, had no effect on the mean plasma concentrations of β-endorphin and prolactin, except under short days when, combined with pimozide, it induced an increase in the plasma concentrations of the two polypeptides. Bromocriptine (0·06 mg/kg, s.c.) caused a significant decrease in the plasma concentrations of both β-endorphin and prolactin; this effect was most marked at the times of increased secretion (under short days for β-endorphin and under long days for prolactin). Sulpiride (0·59 mg/kg, s.c.) produced the converse effect and caused an increase in the plasma concentrations of β-endorphin and prolactin with the amplitude and duration of the effect varying with the stage of the photoperiod-induced cycle. From these results in the Soay ram, we conclude that dopamine inhibits β-endorphin and prolactin secretion by way of D2 receptors under both long and short days. Endogenous opioids interact with dopamine, augmenting this inhibition under short days. Differences in the acute responses in the secretion of β-endorphin and prolactin, and the inverse relationship between β-endorphin and prolactin during the cycle, indicate that different regulatory systems involving dopamine influence the two pituitary polypeptides. Journal of Endocrinology (1990) 127, 461–469


2019 ◽  
Vol 8 (5) ◽  
pp. 571
Author(s):  
Seung Hyun Kim ◽  
Namo Kim ◽  
Eui Hyun Kim ◽  
Sungmin Suh ◽  
Seung Ho Choi

Growth hormone (GH) secretion is regulated by various hormones or neurotransmitters, including gamma-aminobutyric acid. The aim of this study was to determine the propofol requirement in patients with GH-secreting pituitary tumors undergoing transsphenoidal surgery. General anesthesia was induced in 60 patients with GH-secreting tumors (GH group, n = 30) or nonfunctioning pituitary tumors (NF group, n = 30) using an effect-site target-controlled intravenous propofol infusion. The effect-site concentrations were recorded at both a loss of consciousness and a bispectral index (BIS) of 40, along with the effect-site concentration after extubation, during emergence from the anesthesia. The effect-site concentration of propofol was higher in the GH group than in the NF group at a loss of consciousness and a BIS of 40 (4.09 ± 0.81 vs. 3.58 ± 0.67, p = 0.009 and 6.23 ± 1.29 vs. 5.50 ± 1.13, p = 0.025, respectively) and immediately after extubation (1.60 ± 0.27 vs. 1.40 ± 0.41, p = 0.046). The total doses of propofol and remifentanil during anesthesia were comparable between the groups (127.56 ± 29.25 vs. 108.64 ± 43.16 µg/kg/min, p = 0.052 and 6.67 ± 2.89 vs. 7.05 ± 1.96 µg/kg/h, p = 0.550, respectively). The propofol requirement for the induction of a loss of consciousness and the achievement of a BIS of 40 is increased during the induction of general anesthesia in patients with GH-secreting tumors.


Cephalalgia ◽  
1984 ◽  
Vol 4 (4) ◽  
pp. 213-220 ◽  
Author(s):  
Guy Chazot ◽  
Bruno Claustrat ◽  
Jocelyne Brun ◽  
Daniel Jordan ◽  
Geneviève Sassolas ◽  
...  

The temporal organization of plasma melatonin. cortisol. growth hormone (GH) and prolactin secretion was examined in healthy rested controls and in patients suffering from episodic cluster headache. Eleven patients with typical cluster headache (10 men, 1 female) and 8 male controls were studied over a 24–h period: blood was collected at 2–h intervals during the day and at l-h intervals at night. Plasma melatonin. cortisol, GH and prolactin levels were determined by radioimmunoassay. Most of the cluster headache patients showed a decrease in nocturnal melatonin secretion and the melatonin rhythm was even completely abolished in one patient. Chronobiological analysis of the cluster headache patients' 24–h plasma melatonin profile showed a significant decrease in amplitude and mesor: these were 58.7 pg/ml and 34.4 pg/ml respectively in control subjects, versus 18.7 pg/ml and 17.6 pg/ml for the patients. In addition. patients showed a significant phase-advance in their melatonin rhythm For cortisol, the rhythm appeared slightly blunted in the cluster headache group and was significantly phase-advanced. The plasma prolactin profile showed no significant alteration, but for plasma GH the nocturnal peak was advanced in some patients: in the absence of sleep recording, however, no conclusion could be drawn. Results from this study suggest a neuroendocrine dysregulation in cluster headache in the endogenous clock which controls the pineal rhythmicity.


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