Substance P inhibits carbamylcholine-stimulated 22Na+ efflux from acetylcholine receptor-enriched Torpedo electroplaque membrane vesicles.
The effect of substance P on nicotinic acetylcholine receptor function was examined in Torpedo electroplaque membranes. The peptide inhibited carbamylcholine-stimulated 22Na+ efflux in a concentration-dependent manner. By irreversibly blocking spare receptors with alpha-bungarotoxin, the IC50 for substance P was shown to be less than 3 microM. Inhibition by substance P was slow relative to receptor activation by carbamylcholine, consistent with an enhancement of desensitization or a slow allosteric block.
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Department of Pharmacology, New York State College of Veterinary Medicine, Cornell University, Ithaca 14853-6400.
Weiland
G A
GA
D000818:Animals; D002038:Bungarotoxins / Q000378:metabolism; D002217:Carbachol / Q000008:administration & dosage / Q000494:pharmacology*; D002462:Cell Membrane / Q000187:drug effects / Q000378:metabolism; D004557:Electric Organ / Q000187:drug effects / Q000378:metabolism*; D007700:Kinetics; D011978:Receptors, Nicotinic / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*; D012964:Sodium / Q000378:metabolism*; D012979:Sodium Radioisotopes; D013373:Substance P / Q000494:pharmacology*; D014101:Torpedo
D002038:Bungarotoxins; D011978:Receptors, Nicotinic; D012979:Sodium Radioisotopes; D013373:Substance P; D002217:Carbachol; D012964:Sodium