Effects of Alpha- and Beta-Adrenergic Agonists and Antagonists on Growth Hormone Secretion in Man

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Abstract
It is well known that the adrenergic system has both stimulatory and inhibitory influences on growth hormone (GH) secretion probably by modulating GH-releasing hormone (GHRH) and/or somatostatin release. To better understand the mechanisms by which these influences take place, we investigated the effects of .alpha.- and .beta.-adrenergic agonists and antagonists on both basal and GHRH-induced GH release in 23 male adult volunteers. The GH-releasing effect of clonidine (0.15 mg infused iv over 10 min), an .alpha.2-adrenergic agonist, was significantly blunted by yohimbine (30 mg orally at -50 min), a relatively specific .alpha.2-adrenergic antagonist (area under the response curve, mean .+-. SEM, 672.6 .+-. 143.0 versus 219.6 .+-. 16.7 .mu.g/l/h; P < 0.05). On the other hand, the GHRH (1 .mu.g/kg iv as bolus)-induced GH increase was unaffected by yohimbine (339.3 .+-. 19.1 versus 518.1 .+-. 172.8 .mu.g/l/h). Concomitant blockade of .alpha.1/.alpha.2-adrenoreceptors by phentolamine (0.5 mg/ml/min infused iv from -60 to +30 min) abolished the GHRH-induced GH rise (645.5 .+-. 106.0 versus 189.0 .+-. 58.8 .mu.g/l/h; P < 0.01). Finally, the GHRH-stimulated release was blunted by .beta.2-adrenergic stimulation with salbutamol (10 .mu.g/min infused iv from -5 to +15 min) (324.3 .+-. 99.7 versus 112.7 .+-. 48.8 .mu.g/l/h; P < 0.02). In conclsuion: 1) The evidence that yohimbine is able to blunt the clonidine-induced GH release but fails to inhibit the GHRH-induced GH rise indicates that, as in animals, in man too the GH-releasing effect of clonidine is specifically mediated by .alpha.2-receptor activation, and may occur via endogenous GHRH release; 2) the inhibitory effect on GH release of .beta., namely .beta.2, receptor activation is probably mediated by the somatostatinegic system; 3) an unopposed .beta.-adrenergic activation would account for the inhibitory effect on GHRH-induced GH release of concomitant .alpha.1-/.alpha.2-adrenoreceptor blockade by phentolamine.

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