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Evidence that ₂-Adrenergic Pathways Play a Major Role in Growth Hormone (GH) Neuroregulation: ₂-Adrenergic Agonism Counteracts the Inhibitory Effect of Muscarinic Cholinergic Receptor Blockade on the GH Response to GH-Releasing Hormone, while ₂-Adrenergic Blockade Diminishes the Potentiating Effect of Increased Cholinergic Tone on such Stimulation in Normal Men^*

JESUS DEVESA, MARIA J. DIAZ, JESUS A. F. TRESGUERRES, VICTOR ARCE and LUIS LIMA

Laboratorio de Neurociencias "Ramón Domínguez," Department of Physiology, Faculty of Medicine, University of Santiago de Compostela Santiago de Compostela, Spain
The Department of Physiology, Faculty of Medicine, University of Madrid (J.A.F.T.) Madrid, Spain

Address correspondence and requests for reprints to: Prof. J. Devesa, Department of Physiology, Faculty of Medicine, University of Santiago de Compostela, Santiago de Compostela, Spain.

The aim of this study was to investigate the interrelationships between ₂-adrenergic and cholinergic pathways in the control of hypothalamic somatostatin (SRIF) secretion in humans. In eight normal volunteers subjects we compared the pattern of GHRH-induced GH release to that elicited by similar challenge given 60 min after a pretreatment with drugs affecting ₂-adrenergic and muscarinic cholinergic neurotransmission. In a control study, synthetic GHRH [GRF-(l–29); 1 µg/kg, iv] was administered 60 min after giving placebo. In other experiments, the administration of atropine (1 mg, im), or clonidine (0.300 mg, orally), or atropine plus clonidine, or pyridostigmine (120 mg, orally), or yohimbine (30 mg, orally), or pyridostigmine plus yohimbine, at 0 min was followed by GHRH administration 60 min later.

The administration of both clonidine and pyridostigmine significantly (P < 0.01) enhanced the GH responses to GHRH compared to those elicited by this challenge when given after placebo. Conversely, atropine pretreatment significantly (P < 0.01) blocked the GH response to GHRH challenge, whereas yohimbine did not significantly affect it. When atropine and clonidine were given together, the inhibitory effect of the former was overcame and mean GHRH-elicited GH peak response was significantly (P < 0.05) higher than that in the control study. In contrast, pretreatment with yohimbine significantly (P < 0.05) blunted the pyridostigmine-induced enhancement of GHRHelicited GH release. These data confirm our previous postulate suggesting that the stimulatory effect of clonidine on GH release is mainly exerted by inhibiting the hypothalamic SRIF release. Moreover, the effect of cholinergic neurons on SRIF release seems to be, at least in part, dependent on ₂-adrenergic pathways. Based on these data, it can be proposed that the ₂-adrenergic system plays a major role in the control of hypothalamic SRIF release, and hence in GH neuroregulation, whereas the muscarinic cholinergic system would participate in such regulation by modulating the functional activity of the former.

^* This work was supported by a grant from Directión General de Investigatión Científica y Técnica (DGICYT), Ministerio de Educación y Ciencia, Spain (PM88–0208). Presented in part at the second International Congress of Neuroendocrinology, Bordeaux, France, 1990.

Recipients of a grant from Ministerio de Educación y Ciencia (F.P.I.), Spain.

Received May 25, 1990.

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