Beta-Endorphin Mediates Clonidine Stimulated Growth Hormone Release

The role of β-endorphin in the stimulation of growth hormone secretion elicited by administration of clonidine (Clon), an α₂-adrenergic agonist, was investigated in awake, freely moving male rats. Animals were infused slowly with either 1 ml of normal rabbit serum (NRS), β-endorphin antiserum (β-end-AS) or ACTH antiserum (ACTH-AS) 2 h before the administration of Clon (100 µg/kg body weight, intravenously). In addition, naloxone (Nal) (2.5 mg/kg body weight, intravenously) was given 15 min prior to Clon in some experiments. Blood samples were taken at 15-min intervals prior to and following Clon administration. Clon caused plasma GH levels to rise 15-fold to peak levels of 177 ± 38 ng/ml (p < 0.01) at 30 min. Pretreatment of both Nal or β-end-AS significantly reduced Clon-stimulated GH secretion to 72 ± 19 ng/ml (p < 0.05) and 87 ± 30 ng/ml (p < 0.05), respectively. In contrast, the infusion of ACTH antiserum did not affect Clon-stimulated GH release. Our data suggest that β-endorphin or a related opioid peptide is an important mediator of GH secretion induced by α₂-adrenergic stimulation. Since blockade of opioid receptors blunted Clon-induced GH release only partially (approximately 50%), other mediators are most likely activated following cα-adrenergic stimulation.