Noradrenergic Regulation of Growth Hormone Secretion in the Baboon*

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Abstract
We have investigated the effects of iv administered noradrenergic agonists and antagonists on plasma GH concentration in the adolescent baboon, Papio papio, with the aim of defining the relative roles of adrenergic receptor subtypes (α1, α2, β1, and β2) in the regulation of GH release. Clonidine (0.02 mg/kg) or UK-14,304 (0.02 mg/kg), potent centrally acting α2 noradrenergic agonists, were infused into 24 animals pretreated with either saline, or selective α1 and α2 noradrenergic antagonists. Both agonists potently augment plasma GH, producing peak levels of 30–60 ng/ml 15 min post infusion. These responses can be prevented by the prior infusion of the ct2 antagonist, piperoxane (1.0 mg/kg), but not by the α1 antagonist, prazosin (2.0 mg/kg). Log dose response curves of the 2 agonists demonstrate a greater potency for UK-14,304 vs.clonidine on a molar basis. In animals pretreated with monoamine depleting agents (reserpine and α-methyl paratyrosine) the plasma GH response to an infusion of clonidine (0.02 mg/kg) is significantly enhanced (P < 0.001). β-Adrenoreceptor antagonism by propranolol (0.02 or 1.0 mg/ kg) or the more selective β2adrenoreceptor antagonist, ICI 118,551 (0.02–1.0 mg/kg), results in a rapid and significant (P < 0.01) increase in plasma GH. The β1-antagonist, practolol (0.2- 2.0 mg/kg), does not alter plasma GH levels. It is proposed that in the baboon, noradrenaline acts on α2- noradrenergic receptors to stimulate GH release and on β2- noradrenergic receptors to inhibit GH release.