Summary
We sought for presynaptic, release-inhibiting opioid receptors at the postganglionic sympathetic axons innervating the jejunal arteries of rabbits. Evoked excitatory junction potentials (e.j.p.s; trains of 15 pulses at 1 Hz) as well as the evoked overflow of tritium after preincubation with [3H]-noradrenaline (trains of 120 pulses at 1 Hz) were used to estimate transmitter release. In otherwise untreated tissues ethylketocylazocine reduced neither the e.j.p. amplitudes nor the evoked overflow of tritium; [Met5]-enkephalin depressed the evoked overflow of tritium. Ethylketocyclazocine reduced e.j.p. amplitudes, however, in tissues exposed to either yohimbine, tolazoline or phentolamine, but not in tissues exposed to prazosin. Ethylketocyclazocine also depressed the evoked overflow of tritium when yohimbine was present. The inhibition produced by ethylketocyclazocine in the presence of yohimbine was antagonized by (-)-3-furylmethyl)-α-noretazocine (MR 2266) but not by N,N-diallyl-Tyr-α-aminoisobutyric acid-α-aminoisobutyric acid-Phe-Leu-OH (ICI 174864). It is concluded that the sympathetic neurones of rabbit jejunal arteries possess presynaptic κ-receptors in addition to the previously identified δ-receptors. The κ-receptors become operative only when presynaptic α2-adrenoceptors have been blocked.
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Ramme, D., Illes, P., Späth, L. et al. Blockade of α2-adrenoceptors permits the operation of otherwise silent opioid κ-receptors at the sympathetic axons of rabbit jejunal arteries. Naunyn-Schmiedeberg's Arch. Pharmacol. 334, 48–55 (1986). https://doi.org/10.1007/BF00498739
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DOI: https://doi.org/10.1007/BF00498739