Do presynaptic opiate receptors and α-adrenoceptors alter acetylcholine release from a sympathetic ganglion by a similar mechanism?

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The present experiments tested the possible involvement of a calcium-sensitive mechanism in the α-adrenoceptor-and opiate receptor-mediated inhibition of acetylcholine release from the cat superior cervical ganglion. First, the calcium-dependence of evoked acetylcholine release was measured in the presence and absence of the α-adrenoceptor agonist noradrenaline or of the opiate receptor agonist [Met 5]enkephalin-Arg 6-Phe 7. When ganglia were perfused with Krebs medium containing [Ca 2+] = 2.4, 1.2, 0.6, 0.2 mM, evoked release of acetylcholine was depressed by both agonists and the inhibition increased with reduced levels of extracellular Ca 2+; this was especially evident when calcium in the medium was reduced to 0.2 mM. Second, the effects of both noradrenaline and [Met 5]enkephalin-Arg 6-Phe 7 on calcium influx into presynaptic nerve endings was determined by measuring the accumulation of 45Ca into ganglia in the presence and absence of either drug. Both agonists reduced the stimulation-induced increase in 45Ca accumulation. The effect of noradrenaline to reduce calcium influx was blocked by yohimbine or by phentolamine; the effect of [Met 5]enkephalin-Arg 6-Phe 7 to decrease 45Ca accumulation by ganglia was blocked by naloxone. It is concluded that activation of presynaptic opiate receptors and α-adrenoceptors in the cat superior cervical ganglion can alter acetylcholine release by a similar mechanism, i.e. to reduce Ca 2+ influx during preganglionic nerve stimulation.