Inhibition by opioid agonists and enhancement by antagonists of the release of catecholamines from the dog adrenal gland in response to splanchnic nerve stimulation: evidence for the functional role of opioid receptors.

The aim of the present study is to examine how opioid agonists and antagonists modify the splanchnic nerve stimulation (SNS)-induced release of catecholamines from the dog adrenal gland in vivo, in an attempt to elucidate whether opioid receptors play a functional role in controlling catecholamine release. Output of epinephrine (EPI) and norepinephrine (NE) was determined from adrenal venous blood by using high-performance liquid chromatography with electrochemical detection. SNS (0.3, 1 and 3 Hz) produced increases in both EPI and NE output in a frequency-dependent manner. Leu-enkephalin (10-100 micrograms/kg i.v.) and morphine (10-100 micrograms/kg i.v.) attenuated the increase in EPI and NE output induced by 1 or 3 Hz of SNS without affecting the basal catecholamine output. A 25 to 40% reduction of the SNS-induced increase in catecholamine output was observed after the treatment with 100 micrograms/kg of leu-enkephalin or morphine. The increase in EPI and NE output induced by 1 and 3 Hz of SNS was enhanced markedly by naloxone (10-1000 micrograms/kg i.v.) and by naltrexone (10-1000 micrograms/kg i.v.). The SNS-induced increase in catecholamine output doubled after treatment with 100 and 1000 micrograms/kg of naloxone or naltrexone. Basal catecholamine output and the increase in output induced by 1 Hz of SNS were unaffected by naloxone or naltrexone. These results suggest that endogenously released opioid peptides inhibit the release of catecholamines by activating opioid receptors in the adrenal gland of the dog.