Govaerts J, Buydens P, Finné E, Matton A, Vanhaelst L
Laboratory of Pharmacology, Faculty of Medicine and Pharmacy, Free University of Brussels (V.U.B.), Belgium.
J Endocrinol Invest. 1990 Dec;13(11):911-5. doi: 10.1007/BF03349653.
Fentanyl, a selective mu opioid receptor agonist, administered intravenously, influences growth hormone secretion in conscious male rats. A dose-response study demonstrated that the maximum growth hormone release was obtained with 10 micrograms/kg while higher doses were less or not effective. MR-2266 (6 mg/kg i.v.), a mu and kappa opioid receptor antagonist, and bremazocine (0.1 mg/kg i.v.) a mu opioid receptor antagonist with kappa agonistic properties, both potently inhibited the growth hormone response to fentanyl (10 micrograms/kg i.v.). In contrast, the effect of fentanyl on growth hormone release was not blocked in rats treated with either ICI-154129 (30 mg/kg i.v. or 150 micrograms/kg intracerebroventricularly a selective delta opioid receptor antagonist, or U-50488 (10 mg/kg i.v.), a specific kappa opioid receptor agonist. These results suggest that opioid receptors of the mu type are involved in the fentanyl-induced growth hormone release.
芬太尼是一种选择性μ阿片受体激动剂，静脉注射后会影响清醒雄性大鼠的生长激素分泌。一项剂量反应研究表明，静脉注射10微克/千克芬太尼时可实现最大生长激素释放，而更高剂量则效果较差或无效。μ和κ阿片受体拮抗剂MR - 2266（静脉注射6毫克/千克）以及具有κ激动特性的μ阿片受体拮抗剂布瑞马佐辛（静脉注射0.1毫克/千克）均能有效抑制大鼠对芬太尼（静脉注射10微克/千克）的生长激素反应。相比之下，用ICI - 154129（静脉注射30毫克/千克或脑室内注射150微克/千克，一种选择性δ阿片受体拮抗剂）或U - 50488（静脉注射10毫克/千克，一种特异性κ阿片受体激动剂）处理的大鼠中，芬太尼对生长激素释放的作用并未被阻断。这些结果表明，μ型阿片受体参与了芬太尼诱导的生长激素释放。
