Kamei J, Iwamoto Y, Suzuki T, Misawa M, Nagase H, Kasuya Y
Department of Pharmacology, Faculty of Pharmaceutical Sciences, Hoshi University, Tokyo, Japan.
Eur J Pharmacol. 1994 Aug 1;260(2-3):257-9. doi: 10.1016/0014-2999(94)90347-6.
The present study examined the opioid receptors involved in the antitussive effect of dihydroetorphine in mice. Dihydroetorphine suppressed coughs dose dependently at doses between 0.1-1 micrograms/kg i.p. Blockade of mu-opioid receptors by pretreatment with beta-funaltrexamine significantly reduced the antitussive effect of dihydroetorphine. Furthermore, the antitussive effect of dihydroetorphine was also antagonized by nor-binaltorphimine, a kappa-opioid receptor antagonist. However, pretreatment with naltrindole, a delta-opioid receptor antagonist, did not affect the antitussive effect of dihydroetorphine. These results indicate that the antitussive effect of dihydroetorphine is mediated by the activation of mu-opioid receptors and of kappa-opioid receptors, but not delta-opioid receptors.
本研究检测了双氢埃托啡对小鼠镇咳作用所涉及的阿片受体。腹腔注射双氢埃托啡剂量在0.1 - 1微克/千克时，其镇咳作用呈剂量依赖性。用β-芬太尼透皮贴剂预处理阻断μ-阿片受体，可显著降低双氢埃托啡的镇咳作用。此外，κ-阿片受体拮抗剂诺-宾丙诺啡也可拮抗双氢埃托啡的镇咳作用。然而，δ-阿片受体拮抗剂纳曲吲哚预处理并不影响双氢埃托啡的镇咳作用。这些结果表明，双氢埃托啡的镇咳作用是由μ-阿片受体和κ-阿片受体的激活介导的，而非δ-阿片受体。
