Semafuko W E, Follett D L, Dixon W R
Department of Pharmacology and Toxicology, School of Pharmacy, University of Kansas, Lawrence.
Pharmacology. 1988;37(3):195-202. doi: 10.1159/000138463.
The effect of etorphine (ET) on nerve stimulation-mediated release of norepinephrine (NE) was investigated in isolated rat and guinea pig hearts. Hearts were perfused with Krebs bicarbonate solution via the aorta and the overflow of NE was measured after stimulation of the heart. ET (0.001-0.1 mumol/l) caused a dose-dependent inhibition of NE release in both preparations. Inhibition of NE release from guinea pig hearts ranged from 13% at 0.001 mumol/l to 24% at 0.1 mumol/l. The same concentrations of ET decreased NE release by 10 and 36% in the rat heart. The inhibitory effect of ET was blocked by naloxone. It is concluded that presynaptic opioid receptors located on the adrenergic neuronal terminals may be involved in the regulation of adrenergic neurotransmission in the rat and guinea pig heart.
在离体大鼠和豚鼠心脏中研究了埃托啡(ET)对神经刺激介导的去甲肾上腺素(NE)释放的影响。心脏通过主动脉用 Krebs 碳酸氢盐溶液灌注,刺激心脏后测量 NE 的溢出量。ET(0.001 - 0.1 μmol/L)在两种制剂中均引起剂量依赖性的 NE 释放抑制。豚鼠心脏中 NE 释放的抑制率在 0.001 μmol/L 时为 13%,在 0.1 μmol/L 时为 24%。相同浓度的 ET 使大鼠心脏中的 NE 释放分别降低了 10%和 36%。ET 的抑制作用被纳洛酮阻断。得出的结论是,位于肾上腺素能神经元终末的突触前阿片受体可能参与大鼠和豚鼠心脏中肾上腺素能神经传递的调节。