Abstract
Quinidine (2.5 to 5x10(-6) g./ml.) decreased the maximum rate of depolarization of the action potentials (AP) of both isolated rabbit atrial and ventricular fibres recorded with an intracellular microelectrode and finally abolished electrical excitability and spontaneous rhythmicity. Acetylcholine (ACh) 10(-6) restored these properties in the atrium (but not ventricle) without changing the membrane resting potential (MRP). Adrenaline 10(-6) to 10(-4) at the same time was without effect. The maximum rate of depolarization of an AP in response to an extra shock interposed between the 8th and 9th driving stimuli was increased by ACh 10(-6) in atria which had received quinidine to a greater extent than that of the normal AP. It is suggested that ACh restarted atria arrested by quinidine by an action on the sodium "carrying system" (excitatory mechanism) and this was not the result of an increase in MRP. An hypothesis is put forward to explain the stimulatory and inhibitory effects of ACh on rabbit atria.
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