The functional role of opioid receptors in acetylcholine release in the rat adrenal medulla.

The functional role of opioid receptors in acetylcholine release from splanchnic nerve terminals in the adrenal medulla was investigated in halothane-anesthetized rats. The extracellular acetylcholine level was measured by a newly developed in vivo adrenal microdialysis method. The potassium (K+)-evoked acetylcholine release from the splanchnic nerve terminals was inhibited by morphine (10 microM), a mu-opioid receptor agonist, and [D-Pen2,D-Pen5]enkephalin (DPDPE, 1 and 10 microM), a delta-opioid receptor agonist. These inhibitory effects of morphine and DPDPE were significantly abolished by naltrexone (9 mg/kg i.p.), a mu-opioid receptor antagonist, and naltrindole (9 mg/kg i.p.), a delta-opioid receptor antagonist, respectively. 5 alpha,7 alpha-beta-(-)- N-methyl-N-[7-(1-pyrrolidinyl)-1-oxaspiro(4,5)dec-8-yl]benzene acetamide (U69593, 10 microM), a kappa-opioid receptor agonist, had no influence on the K(+)-evoked acetylcholine release. The findings suggest that both mu- and delta-opioid receptors might have a functional role in acetylcholine release from splanchnic nerve terminals in the adrenal medulla of the rat. The present study indicates that adrenal microdialysis is a useful method for studying the control mechanism of adrenomedullary function in the rat in vivo.