CATECHOLAMINERGIC MEDIATION OF MORPHINE-INDUCED ACTIVATION OF PITUITARY-ADRENOCORTICAL AXIS IN THE RAT - IMPLICATION OF ALPHA-ADRENOCEPTORS AND BETA-ADRENOCEPTORS

The present study investigates the role of hypo thalamic catecholamines in the effects of morphine on hypothalamo-pituitary-adrenocortical (HPA) axis. Acutely administered morphine (30 mg/kg i.p) increased plasma corticosterone and reduced the hypothalamic noradrenaline (NA) content but it did not change either the dopamine (DA) concentration or the ratio DOPAC/DA. After reserpine administration the hypothalamic contents of NA and DA were drastically reduced without changing plasma corticosterone concentrations. The increase in plasma corticosterone induced by morphine was significantly reduced by the pretreatment with reserpine. The alpha(1)- and alpha(2)-antagonists prazosin and yohimbine, respectively, significantly antagonized the effect of morphine on plasma corticosterone. The beta-antagonist propranolol also significantly attenuated the increase of corticosterone secretion induced by morphine. The results suggest that the action of the opiate on HPA axis activity may be dependent on stimulatory catecholaminergic systems which utilize alpha(1)-, alpha(2)- and beta-adrenoceptors.