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INHIBITORY ROLE OF THE SEROTONINERGIC SYSTEM IN HYPOGLYCAEMIA-INDUCED GROWTH HORMONE RELEASE IN THE DOG

1976; Oxford University Press; Volume: 82; Issue: 1 Linguagem: Inglês

10.1530/acta.0.0820071

1479-683X

E. E. Müller, G. Udeschini, C. Secchi, F. Zambotti, A. E. Panerai, L. Vicentini, F. Cocola, Paolo Mantegazza,

Pancreatic function and diabetes

The effect of functional activation of the serotoninergic system on base line plasma growth hormone (GH) levels and the participation of serotonin (5-HT) in the GH response evoked by insulin-induced hypoglycaemia were studied in the unanaesthetized dog with the aid of a specific and sensitive homologous radioimmunoassay method. In 4 dogs, intravenous injection of insulin (0.4 IU/kg iv) or infusion of L-tryptophan (TP, 2.0 g over 30 min) showed the latter stimulus to be by far less potent in eliciting growth hormone (cGH) release. Intravenous injection of L-5-hydroxytryptophan (5-HTP, 10 mg/kg iv) in 5 dogs induced a clear-cut rise in cGH, but was accompanied by striking side effects. In 9 dogs, administration of p-chlorophenylalanine (PCPA, 100 mg/kg po daily × 5 days), an inhibitor of 5-HT synthesis, did not modify base line cGH and glucose levels, caused a marked decrease of blood 5-HT and resulted in a magnification of the insulin-induced cGH release. In 8 dogs, similarly treated with PCPA, administration of 5-HTP (10 mg/kg iv), 10 min before the hypoglycaemic stimulus, blunted the GH secretory response to the latter. Chronic feeding of a TP-deficient diet in 5 dogs, was accompanied by a progressive decrease of total and "free" plasma TP, no significant changes in base line cGH and blood glucose levels and a GH response to the insulin stimulus (0.2 IU/kg iv) almost super-imposable to that elicitable in the same animals under normal conditions. TP infusion (2.0 g over 30 min) in 3 TP-deficient dogs, induced a striking reduction of the hypoglycaemia-induced GH release. Collectively, this study suggests that 5-HT does not have a noticeable effect on base line plasma cGH levels but exerts an inhibitory role in hypoglycaemia-induced cGH release.