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Unité de Neuroendocrinologie, INSERM, U.159, 2 ter Rue d'Alesia, 75014 Paris, France
(Received 16 August 1977)
It is known that catecholamines play an important role in the regulation of growth hormone (GH) secretion, but the effects of dopamine and alpha- and beta-adrenergic agonists on the release of GH in the rat are controversial (Collu, Fraschini, Visconti & Martini, 1972; Kato, Dupre & Beck, 1973; Durand, Martin & Brazeau, 1977). It has been proposed (Bluet-Pajot, Schaub & Nassiet, 1976; Bluet-Pajot & Schaub, 1977; Durand et al. 1977) that the conflicting data obtained in the rat may be due to the anaesthesia; most of the GH responses reported to be atypical in the rat, compared with those of primates, were obtained under urethane anaesthesia, which is known to result in long-lasting and irreversible endocrine imbalance.
In contrast, neurotransmitters or experimental hypoglycaemia do not appear to induce paradoxical GH responses in rats treated
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Unité de Neuroendocrinologie, INSERM – U.159, 2ter rue d'Alésia, 75014 Paris, France
(Received 16 February 1977)
It has been reported by Kokka, Garcia, George & Elliott (1972) and Martin, Audet & Saunders (1975) that morphine stimulates the release of growth hormone (GH) in the rat. Previous studies from this laboratory indicated that another narcoanalgesic, gamma-hydroxybutyrate (GHB), is able to stimulate immunoreactive GH secretion, but the pattern of this response differs markedly from that elicited by morphine (M. T. Bluet-Pajot & C. Schaub, unpublished results). We have also used GHB and eliminated stress effects to demonstrate that GH secretion in the rat can be induced by controlled hypoglycaemia as in primates (Bluet-Pajot, Schaub & Nassiet, 1976).
In the present study we have investigated whether morphine could elicit a GH response under GHB narcoanalgesia, and whether GH secretion induced by spontaneous or provoked hypoglycaemia interfered with this effect.
Automated blood glucose monitoring
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ABSTRACT
The effects of dopamine on GH release were investigated both in vivo in freely moving intact rats and in rats with a mediobasal hypothalamic lesion, and in vitro in a perifusion system using dispersed male rat pituitary cells kept in primary culture. In vivo, dopamine (5 mg/kg body weight) induced a rapid and very transient increase in plasma GH levels in lesioned but not in intact rats. This increase was markedly inhibited by a prior injection of the D1 antagonist SCH 23390 (0·5 mg/kg) but not of the D2 antagonist domperidone (0·5 mg/kg). The D, agonist SKF 38393 induced a dose-dependent stimulation of GH release in lesioned rats, and the effect obtained with a dose of 5 mg/kg was abolished by pretreatment with SCH 23390 (0·5 mg/kg). In vitro, dopamine (0·1 μmol/l) and SKF 38393 (0·1 μmol/l) provoked a rapid and reversible release of GH from superfused rat pituitary cells; this effect was markedly inhibited by simultaneous superfusion of SCH 23390 (1 μmol/l). These findings indicate that dopamine can stimulate basal GH release at the pituitary level and that this stimulation is mediated by D1 but not by D2 receptors. They also support the hypothesis that unidentified hypothalamic neurohormones may modulate this effect.
Journal of Endocrinology (1990) 127, 191–196
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The β-adrenergic agonist, isoprenaline, and antagonist, propranolol, had no effect on the delayed basal secretion of GH consistently observed in rats treated with the narco-analgesic gamma-hydroxybutyrate. Under the same experimental conditions, GH release was distinctly stimulated by infusion of the α-adrenergic agonist, clonidine, and by morphine; both responses were dose-dependent. The effects of β-adrenergic agonists and antagonists on these GH responses were as follows: in rats pretreated with isoprenaline the GH release induced by clonidine and morphine was abolished whereas it was enhanced in rats pretreated with propranolol. These data confirmed and extended previous reports from this laboratory on the inhibitory role of β-adrenergic receptors on GH regulation.
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Involvement of endogenous corticotropin releasing hormone (CRH) in the regulation of spontaneous growth hormone (GH) secretion was investigated. A CRH antagonist, α helical CRH 9–41, was intracerebroventricularly infused for 36 h at a rate of 1 μg/0·5 μl/h to freely moving, cannulated adult male rats. Serial blood samples were drawn every 20 min for the last 8 hours of α helical CRH 9–41 infusion. The treatment induced a marked increase in GH peak amplitude without affecting either trough levels or numbers of peaks. In parallel, levels of growth hormone releasing hormone (GHRH) mRNA in the arcuate nucleus, but not of somatotropin release inhibiting hormone (SRIH) mRNA in the periventricular and arcuate nuclei, were increased. These data suggest that, in addition to its action in the stress-induced inhibition of GH secretion through regulation of periventricular SRIH neurons, CRH can also act as a modulator of endogenous GH secretion through regulation of arcuate GHRH neurons. Whether the modulatory effects of CRH on GHRH neurons are direct or indirect remains to be established.
Journal of Endocrinology (1997) 152, 431–436
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The administration of gamma-hydroxybutyrate (GHB) induced a consistent secretory episode of growth hormone (GH) in the morning followed by basal levels of secretion of GH for several hours. The measurement of endogenous noradrenaline, dopamine and serotonin (5-HT) following infusion of GHB showed that dopamine concentrations were significantly increased in the striatum; at the level of the hypothalamus, however, no significant differences were observed between control and GHB-treated animals.
The data reported in this study are consistent with the interpretation that the neurotransmitter regulation of GH release and the modulation of hypothalamic gluco-receptor systems are not fundamentally different in rodents and primates.
Clonidine, an α-adrenergic agonist, enhanced the peak of GH observed in the morning and caused a rapid increment of GH during the period when it was normally at basal levels. Under the same experimental conditions, dopamine agonists, apomorphine and levodopa, had no effect on GH secretion. The inhibition of catecholamine synthesis by α-methyl-p-tyrosine blocked the secretory episode of GH following administration of GHB and after insulin hypoglycaemia whereas the GH rise induced by clonidine was unchanged. The inhibition of 5-HT synthesis by p-chlorophenylalanine also suppressed the secretory episode of GH seen in the morning and the release of GH induced by hypoglycaemia; both being partly restored in animals pretreated with 5-hydroxytryptamine.
