Effects of opioid compounds on desensitization of the nicotinic response of isolated bovine adrenal chromaffin cells.

Opioid compounds have been assessed for their ability to modify desensitization of nicotine-induced catecholamine secretion from cultured, bovine, adrenal chromaffin cells. Dynorphin-1-13 and metorphamide produced protection against desensitization of the nicotinic response at concentrations between 1 and 20 microM while etorphine and morphine only produced this effect at 100 microM. The opioid antagonists, naloxone and diprenorphine, at 100 microM mimicked the weak ability of the opioid agonists to protect against nicotinic desensitization. All opioid compounds tested were considerably more potent at inhibiting nicotine-induced catecholamine secretion from the cells than at protecting against desensitization of this response. It is concluded that adrenal opioid peptides probably do not act on adrenal opioid binding sites characterised from ligand binding studies to prevent the nicotinic response from desensitizing. They are unlikely, therefore, to be involved in such a mechanism to maintain catecholamine secretion during stress.