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In the guinea-pig superior cervical ganglion, the Gi blocking agent sulmazole enhanced the basal and prostaglandin E2-induced stimulation of cyclic AMP synthesis but had no effect on the prostaglandin-dependent inhibition of acetylcholine release. On the contrary sulmazole counteracted the inhibitory effect of D-Ala2-Met-enkephalinamide both on cyclic AMP formation and acetylcholine release. Moreover sulmazole eliminated the supra-additive effect of the combination of prostaglandin + opiate on cyclic AMP synthesis. The presence of a Gi-coupled opiate receptor at the pre-and postsynaptic levels is suggested.
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