Marley P D, Livett B G
Biochem Pharmacol. 1987 Sep 15;36(18):2937-44. doi: 10.1016/0006-2952(87)90206-1.
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.
已对阿片类化合物调节尼古丁诱导的培养牛肾上腺嗜铬细胞儿茶酚胺分泌脱敏作用的能力进行了评估。强啡肽-1-13和甲硫酰胺在1至20微摩尔浓度下可防止烟碱反应脱敏，而埃托啡和吗啡仅在100微摩尔时产生此效应。阿片类拮抗剂纳洛酮和二丙诺啡在100微摩尔时模拟了阿片类激动剂防止烟碱脱敏的微弱能力。所有测试的阿片类化合物在抑制尼古丁诱导的细胞儿茶酚胺分泌方面比防止该反应脱敏的效力要强得多。得出的结论是，肾上腺阿片肽可能不会作用于配体结合研究中表征的肾上腺阿片结合位点，以防止烟碱反应脱敏。因此，它们不太可能参与在应激期间维持儿茶酚胺分泌的这种机制。
