Abstract
Spontaneous action potential (AP) discharge could be induced by an application of long (5-10 sec) depolarizing currents in 68% of canine ventricular myocardium tested in the voltage range between about -65 and-10mV. The constant currents of various intensities were applied across a sucrose gap, and intracellular potentials were recorded with a microelectrode. The firing rate of the AP's was voltagedependent and ranged between 0.7 and 2.5Hz. The AP was dependent on both [Ca++]0 and [Na+]0. Increase of [Na+]0 from 37 to 149mM increased the firing rate, maximum rate of rise, and overshoot of the AP's while increase of [Ca++]0 from 0.45mM to 1.8 and 7.2mM increased the firing rate and maximum rate of rise, but did not change the amplitude of overshoot. AP discharges were not blocked by tetrodotoxin (10-5Gm/ml), but were effectively blocked by verapamil (6×10-6Gm/ml). Adrenaline (5×10-6Gm/ml) initiated AP's in otherwise quiescent preparations. The results suggest that spontaneous AP's may be produced by inflowing of slow Na+ and Ca++ currents modified by underlying change of K+-permeability. Possible clinical significance of this phenomenon is discussed in relation to ventricular arrhythmia.
