The effects of aconitine upon the cardiac membrane potential were investigated on the ventricular muscle of the dog by means of the intracellular microelectode technique.
Aconitine produces ectopic, spontaneous and repetitive activity of the cardiac cell on which it acts. By recording the changes in membrane potential throughout the whole course from the moment of application of the drug until the onset of the spontaneous activity of the induced pacemaker, it has been confirmed that aconitine makes manifest, and enhances the latent tendency of the cell to have an oscillatory potential following the spike, and that the oscillatory swing touches off the spontaneous spike after having been augmented to a definite critical level by repeated excitaions. At least several drives have to be given consecutively before the enhanced oscillatory potential attains to the critical level.
In the ordinary pacemaker cell of the heart which is functioning as such, aconitine accelerates progressively its spontaneous slow depolarization, and produces extremely rapid tachycardia, flutter and fibrillation.
Ca and Mg ions counteract the aconitine action. At concentrations higher than normal, both of these ions inhibit or prevent the spontaneous activity due to aconitine.
The implications of these effects of aconitine in the mechanism of production of the spontaneous activity of the natural pacemaker cells are discussed.