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.
D000255:Adenosine Triphosphate / Q000494:pharmacology*; D000818:Animals; D002038:Bungarotoxins / Q000494:pharmacology; D002217:Carbachol / Q000494:pharmacology; D002478:Cells, Cultured; D002642:Chick Embryo; D003470:Culture Media; D009132:Muscles / Q000294:innervation / Q000378:metabolism*; D011868:Radioisotopes / Q000378:metabolism*; D011950:Receptors, Cholinergic / Q000187:drug effects*; D012413:Rubidium / Q000378:metabolism*; D009435:Synaptic Transmission / Q000187:drug effects; D014403:Tubocurarine / Q000494:pharmacology
D002038:Bungarotoxins; D003470:Culture Media; D011868:Radioisotopes; D011950:Receptors, Cholinergic; D000255:Adenosine Triphosphate; D002217:Carbachol; D012413:Rubidium; D014403:Tubocurarine