Abstract
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 mug/l/h; P<0.05). On the other hand, the GHRH (1 mug/kg iv as a bolus)-induced GH increase was unaffected by yohimbine (339.3 +/- 19.1 versus 518.1+/-172.8 mug/I/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 mug/l/h; P<0.01). Finally, the GHRH-stimulated release was blunted by beta(2)-adrenergic stimulation with salbutamol (10 mug/min infused iv from -5 to +15 min) (324.3 +/- 99.7 versus 112.7 +/- 48.8 mug/l/h; P<0.02). 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 somatostatinergic 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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