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.