Abstract
The effect of acetylcholine on the aconitine induced delayed afterdepolarisation and triggered electrical activities under nominally calcium free conditions were studied in frog atrium and ventricle. The changes in intracellular potassium activity were also examined. The aconitine induced delayed afterdepolarisation and triggered electrical activities in atrial muscles were transiently suppressed by acetylcholine. This inhibition was correlated with the time course of the development of hyperpolarisation in the resting membrane potential during acetylcholine application. Propranolol did not abolish the transient inhibition of delayed afterdepolarisation during continuous application of acetylcholine, whereas atropine completely inhibited this effect of acetylcholine. Intracellular potassium activity decreased with time after acetylcholine application, whereas the resting potential became hyperpolarised at an early stage, showing slow recovery thereafter. These results indicate that the transient inhibition of delayed afterdepolarisation by acetylcholine is associated with transient hyperpolarisation of the membrane potential, which is assumed to be caused by potassium accumulation or desensitisation of the muscarinic receptor, or both.
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