ATP-induced cation influx in myotubes is additive to cholinergic agonist action.

Using biochemical methods, ATP was shown to induce an inward flux of 86Rb into cultured chick myotubes. A biphasic dose-response curve was observed, the first part of which was saturable and had an EC50 value of approximately 10 microM. beta, gamma-imido ATP inhibited the ATP-induced uptake. ADP, AMP and adenosine were less potent than ATP in producing influx. ATP-induced influx of 86Rb was found to be additive to carbachol-induced influx and, in contrast to the latter, not blocked by the nicotinic acetylcholine receptor antagonist alpha-bungarotoxin. The results suggest the presence of an ATP recognition-site on myotubes, triggering ion-permeation.