Presynaptic opioid receptors in the rabbit ear artery.
The effect of opioids was compared on field stimulation-induced 3H-noradrenaline overflow and vasoconstriction in the rabbit ear artery. Subtype-selective opioids were used, namely the mu-receptor agonist morphine, the delta-receptor agonist Leu-enkephalin and the kappa-receptor agonists ethylketocyclazocine and dynorphin1-13. Morphine (10 and 100 microM) exerted no inhibitory effect. The delta- and kappa-agonists depressed both the stimulation-evoked overflow and the vasoconstrictor responses with a similar potency. Naloxone prevented the effect of the respective agonists and in the same concentration range (3-10 microM) slightly increased transmitter release. During a continuous exposure of the preparation to Leu-enkephalin (0.1 microM) specific desensitization developed towards a higher concentration of this neuropeptide (1 microM), whereas the inhibition produced by ethylketocyclazocine (1 x microM) was unaffected. Exogenous and endogenous opioids may modulate transmitter release and in consequence vasoconstriction in the rabbit ear artery by acting on neuronal delta- and kappa-receptors.
D000818:Animals; D001158:Arteries / Q000502:physiology*; D004423:Ear / Q000098:blood supply; D004558:Electric Stimulation; D004743:Enkephalin, Leucine / Q000494:pharmacology*; D009638:Norepinephrine / Q000494:pharmacology; D011817:Rabbits; D011957:Receptors, Opioid / Q000502:physiology*; D013569:Synapses / Q000502:physiology; D014661:Vasoconstriction / Q000187:drug effects
D011957:Receptors, Opioid; D004743:Enkephalin, Leucine; D009638:Norepinephrine