Comparison of the effect of insulin hypoglycemia and clonidine on secretion of growth hormone, cortisol and beta-endorphin in children and adolescents.

Plasma beta-endorphin, human growth hormone (hGH) and cortisol were measured concomitantly during insulin hypoglycemia (0.1 u/kg i.v.) or clonidine administration (0.075 mg/m2 orally) in children with idiopathic short stature. Whereas hypoglycemia raised plasma beta-endorphin levels, clonidine slightly decreased beta-endorphin in six subjects and had no effect in four. Cortisol levels increased following hypoglycemia and decreased markedly after clonidine. hGH increased to greater than 20 ng/ml in all but one subject. The findings are interpreted as further evidence that the hGH stimulation of clonidine is not stress-mediated.

Effect of clonidine on plasma beta-endorphin, cortisol and growth hormone secretion in opiate-addicted subjects.

The effect of clonidine on plasma beta-endorphin, cortisol and growth hormone was studied in nine opiate-addicted subjects and seven control subjects aged 15 to 37 years. Clonidine, 0.15 mg, was administered orally in the morning, 18 to 24 h after the last administration of opioid drugs. Basal morning beta-endorphin levels were lower in the addicted than in the control subjects (3.76 +/- 0.8 vs. 7.42 +/- 1.2 pmol/l). Following the clonidine, there was an increase to normal values in the addicted subjects, but in the control subjects there was no change. Basal morning levels of cortisol were higher in the addicted subjects than in the controls (21.0 +/- 3.6 micrograms/dl vs. 13.0 +/- 1.2 microgram/dl, mean +/- SE). In control subjects clonidine induced a decrease of 50% in plasma cortisol, whereas in addicted subjects the decrease was not significant. It is hypothesized that in addicted subjects there is impaired activity of endogenous opioid peptides, leading to alteration in beta-endorphin and cortisol secretion.