흰쥐 적출관류 부신에서 선택적인 nicotine 수용체 효능약인 DMPP(1,1-dimethyl-4-phenylpiperazinium)와 acetylcholine(ACh)의 카테콜아민(CA) 분비작용에 대한 opioids의 영향을 연구하고자 시행하여 얻어진 연구결과는 다음과 같다. Methionine-enkephalin(9.68 × 10-6 M)으로 전처치시 DMPP(100 uM)과 ACh(50μg)에 의한 CA 유리작용이 현저히 억제되었으며 basal CA release는 영향을 받지 않았다. Morphine(1.73 × 10-5 M)으로 전처치시 DMPP 및 excess K+의 CA 분비작용은 뚜렷이 약화되었다. Morphine 역시 그자체는 basal CA release에는 영향을 미치지 않았다. Opiate 수용체 길항제인 naloxone(1.22 × 10-7 M)은 DMPP 및 ACh에 의한 CA 분비작용을 현저히 차단 하였으나 basal CA release에는 영향을 미치지 못하였다. 이와 같은 연구결과로 보아, 흰쥐 관류 부신에서 니코틴 수용체에 의한 CA 분비작용은 내인성 opioid peptide에 의해서 억제되며, 이는 부신에 존재하는 opiate 수용체 흥분작용에 기인되는 것으로 사료된다.
The present study was conducted to investigate the effect of opioids on catecholamine (CA) secretion evoked by a selective cholinergic nicotinic agonist, 1,1-dimethyl-4-phenyl piperazinium (DMPP) and acetylcholine from the retrogradely perfused rat adrenal glands. Methionine-enkephalin (9.68 × 10-6 M) caused a significant inhibition of CA secretion evoked by DMPP (100 uM) and ACh (50μg), but had no effect on the spontaneous (basal) CA release. Morphine (1.73 × 10-5 M) attenuated considerablely the increase in CA release induced by DMPP and ACh. Morphine itself also did not affect the basal CA output. A 20 to 65% reduction of the DMPP- and ACh-evoked increase in CA release was observed after the pretreatment with methionine-enkephalin or morphine. The increase in CA release evoked by DMPP and ACh was reduced markedly by preloading with an opiate antagonist naloxone (1.22 × 10-7 M) while basal CA output was not affected by naloxone. These present experimental results suggest that the nicotinic stimulation-evoked CA release from the perfused rat adrenal gland is inhibited by endogenously released opioid peptides through activation of opiate receptors located in the adrenal gland.
