Effects of Metoclopramide on the Growth Hormone Response to Galanin in Normal Man

 

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Summary

One of the most prominent metabolic effects of the systemic administration of the synthetic neuropeptide galanin in man is the increase in growth hormone (GH) secretion. This stimulating action of galanin is thought to occur directly at the hypothalamic level through the release of GHRH. Recently, it has been shown that also dopaminergic drugs may elicit GH secretion through an increase in hypothalamic GHRH secretion. The aim of this study was to investigate if the action of galanin on GHRH and consequently on GH release may be mediated via dopaminergic pathways evaluating the effects of a potent central dopaminergic receptor blocker, metoclopramide (MCP), on the galanin-induced growth hormone (GH) secretion in normal subjects. We studied seven young non obese healthy subjects (three females and four males). GH secretion was evaluated after 45 min iv infusion of porcine galanin (0.5 mg in 100 ml of saline) from 0 to 45 min combined with a 60 min iv infusion of a) saline (100 ml) or b) MCP (l0 mg in 100 ml of saline) from -15 to 45 min. In all the seven subjects, during galanin infusion, GH values increased with respect to baseline with peaks occurring between 30 and 60 min after the beginning of galanin infusion. Peak GH values ranged between 3.5 and 15.4 μg/l (mean 10.4 ± 1.6 μg/l). During MCP infusion no significant differences in the GH response to galanin with respect to saline were observed both when absolute GH levels and GH AUC were examined. In all the subjects GH levels were increased with respect to baseline level with peaks ranging from 4.7 to 20.3 μg/l (mean 10.6 ± 2.1 μg/l) and occurring between 30 and 60 min after the beginning of galanin infusion. Thus, we conclude that galanin does not elicit GH secretion interacting at the central nervous system level with dopaminergic receptors. It can be hypothesized that galanin interacting with its own receptors may activate at the hypothalamic level GHRH neurons either directly or indirectly through neurotransmitters other than dopamine.