Morphine-induced supersensitivity to acetylcholine in skeletal muscle and its mechanism of action.
The effect of in vitro morphine pretreatment (250 micron) on the sensitivity of skeletal muscle to acetylcholine (ACh) was investigated using the isolated rectus abdominis muscle of frog. Morphine (15 to 120 min) significantly increased the sensitivity of the tissue to ACh. This increase in the sensitivity was found to be greatest after 120 min. Morphine significantly increased the sensitivity of the tissue to carbachol only after 120 min. In the presence of physostigmine, morphine did not cause further augmentation of responses to ACh. Potassium chloride-induced contractile responses were not influenced by morphine. In the presence of morphine, maximum contractile responses to ACh were significantly decreased. Highly calcium (1.62 mM) in the medium decreased the magnitude of the morphine-induced supersentivity to ACh at 120 min and antagonised the decrease in maximum contractile responses to ACh. These results suggest that morphine is causing supersensitivity by both its anticholinesterase activity and its inhibitory action on presynaptic nerve terminals.
D000109:Acetylcholine / Q000494:pharmacology*; D000818:Animals; D001001:Anura; D002118:Calcium / Q000494:pharmacology; D002217:Carbachol / Q000494:pharmacology; D004357:Drug Synergism; D066298:In Vitro Techniques; D009020:Morphine / Q000494:pharmacology*; D009119:Muscle Contraction / Q000187:drug effects*; D010830:Physostigmine / Q000494:pharmacology; D011189:Potassium Chloride / Q000494:pharmacology
D011189:Potassium Chloride; D009020:Morphine; D002217:Carbachol; D010830:Physostigmine; D000109:Acetylcholine; D002118:Calcium