Beta-endorphin mediates clonidine stimulated growth hormone release

The role of beta-endorphin in the stimulation of growth hormone secretion elicited by administration of clonidine (Clon), an alpha2-adrenergic agonist, was investigated in awake, freely moving male rats. Animals were infused slowly with either 1 ml of normal rabbit serum (NRS), beta-endorphin antiserum (beta-end-AS) or ACTH antiserum (ACTH-AS) 2 h before the administration of Clon (100 microgram/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 less than 0.01) at 30 min. Pretreatment of both Nal or beta-end-AS significantly reduced Clon-stimulated GH secretion to 72 +/- 19 ng/ml (p less than 0.05) and 87 +/- 30 ng/ml (p less than 0.05) respectively. In contrast, the infusion of ACTH antiserum did not affect Clon-stimulated GH release. Our data suggest that beta-endorphin or a related opioid peptide is an important mediator of GH secretion induced by alpha2-adrenergic stimulation. Since blockade of opioid receptors blunted Clon-induced GH release only partially (approximately 50%), other mediators are most likely activated following alpha 2-adrenergic stimulation.