Abstract
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.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Acetylcholine / metabolism
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Adenylyl Cyclases / metabolism
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Adipose Tissue / drug effects
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Animals
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Cardiotonic Agents / pharmacology*
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Cyclic AMP / biosynthesis*
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Dinoprostone / pharmacology*
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Dose-Response Relationship, Drug
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Enkephalin, Methionine / analogs & derivatives*
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Enkephalin, Methionine / pharmacology
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GTP-Binding Proteins / metabolism
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Ganglia, Sympathetic / drug effects
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Ganglia, Sympathetic / metabolism*
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Guinea Pigs
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Imidazoles / pharmacology*
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In Vitro Techniques
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Kinetics
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Neurotransmitter Agents / metabolism*
Substances
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Cardiotonic Agents
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Imidazoles
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Neurotransmitter Agents
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Enkephalin, Methionine
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enkephalinamide-Met, Ala(2)-
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Cyclic AMP
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GTP-Binding Proteins
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Adenylyl Cyclases
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sulmazole
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Dinoprostone
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Acetylcholine