Properties of an acetylcholine-induced conductance in the rabbit atrial myocardium.
Using a conventional microelectrode technique, action potentials (A.P.) recorded from the isolated left atrial trabeculae of the rabbit were analyzed. The membrane current during A.P. was reconstructed. In spite of an extracellular Ca2+-deficiency and the application of verapamil, acetylcholine (ACh) reduced the A.P. duration by inducing an outward current IACh. This current was blocked by atropine (10-6 M). A Nernst-plot of the reversal potential at different K+-concentrations showed a slope of 58.5 mV for a 10-fold change in concentration. After pacing pauses longer than 10 s an inward going (anomalous) rectification (A.R.) for IACh occurred. Increasing the duration of the pacing pauses the rectification was more accentuated. During a constant pacing the A.R. for IACh disappeared. ACh did not modify the A.R. The maximum slope conductance for IACh was dependent on the extracellular concentration of ACh (0.035 mS x cm-2 at 20 microM ACh, 0.012 mS x cm-2 at 0.2 microM ACh). The experimental results are discussed, using the model of an ACh-induced potassium channel. The channel should be related to the muscarinic receptor of the atrial myocardium.
D000109:Acetylcholine / Q000494:pharmacology*; D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D016275:Atrial Function; D001285:Atropine / Q000494:pharmacology; D002462:Cell Membrane / Q000187:drug effects / Q000502:physiology; D006325:Heart Atria / Q000187:drug effects*; D066298:In Vitro Techniques; D007473:Ion Channels / Q000187:drug effects; D008564:Membrane Potentials / Q000187:drug effects; D008839:Microelectrodes; D011188:Potassium / Q000378:metabolism; D011817:Rabbits; D014700:Verapamil / Q000494:pharmacology
D007473:Ion Channels; D001285:Atropine; D014700:Verapamil; D000109:Acetylcholine; D011188:Potassium