Vollmar A M, Arendt R M, Schulz R
Institut für Pharmakologie, Toxikologie und Pharmazie der Tierärztlichen Fakultät der Universität München, F.R.G.
Eur J Pharmacol. 1987 Nov 17;143(3):315-21. doi: 10.1016/0014-2999(87)90455-9.
The effect of multiple opioid receptor agonists on plasma immunoreactive atrial natriuretic factor (IR-ANF) was studied in conscious non-hydrated rats. We found that mu-opioid receptor agonists, given subcutaneously, increased plasma IR-ANF, while kappa-receptor agonists did not alter the plasma levels of IR-ANF. The mu-agonist fentanyl (0.05 mg/kg) caused a 10-fold increase in the concentration of IR-ANF, maximal levels being reached within 5-10 min. U 50,488-H and ethylketocyclazocine (EKC), both selective kappa-receptor ligands, were ineffective in this respect. The effect of fentanyl upon plasma IR-ANF was completely abolished by pretreatment with the narcotic antagonist naltrexone, proving opioid receptor specificity of the fentanyl effect. The quaternary antagonist N-methylnaltrexone (1 mg/kg) failed to block the fentanyl-induced increase of ANF, suggesting that opiates bring about their action on ANF via a central mechanism.
在清醒未水化的大鼠中研究了多种阿片受体激动剂对血浆免疫反应性心房利钠因子(IR-ANF)的影响。我们发现,皮下给予μ-阿片受体激动剂会增加血浆IR-ANF,而κ-受体激动剂不会改变IR-ANF的血浆水平。μ-激动剂芬太尼(0.05mg/kg)使IR-ANF浓度增加了10倍,在5-10分钟内达到最高水平。U 50,488-H和乙基酮环唑辛(EKC)这两种选择性κ-受体配体在这方面均无效。用麻醉拮抗剂纳曲酮预处理可完全消除芬太尼对血浆IR-ANF的影响,证明了芬太尼作用的阿片受体特异性。季铵拮抗剂N-甲基纳曲酮(1mg/kg)未能阻断芬太尼诱导的ANF增加,表明阿片类药物通过中枢机制对ANF产生作用。