Nature of "residual fast channel" dependent action potentials and slow conduction in guinea pig ventricular muscle and its modification by isoproterenol.

The nature of "residual fast channel" dependent action potentials and conduction was studied in guinea pig ventricular papillary muscle in which the resting potential was reduced to 58 +/- 1 mV in high K+ (16.7 mM) Tyrode's solution, with or without isoproterenol (0.1 microM). In the absence of isoproterenol, the action potential had a slur on the upstroke and the maximum rate of rise (Vmax) was composed of 2 separable peaks: the early large (32 +/- 7 V/s, Vmax,fast) and the late small (10 +/- 2 V/s, Vmax,slow) ones. The conduction velocity ranged from 30 to 35 cm/s. The Vmax,fast was selectively depressed by l-verapamil (1 microgram/ml), indicating that the impulses were transmitted through incompletely inactivated ("residual") fast channels. Lidocaine (2 micrograms/ml) depressed Vmax,fast with reduction of conduction velocity to about 20 cm/s just before the conduction block. Isoproterenol quadrupled the Vmax,slow but decreased Vmax,fast. As a result, the Vmax,slow overrode the Vmax,fast without change in the conduction velocity. In the absence of isoproterenol, there was no rate-dependent change in the action potential duration and the effective refractory period among the rates of 0.1, 0.5, and 0.9 Hz. Isoproterenol produced rate-dependent shortening in action potential duration with rate-independent shortening of postexcitation refractoriness, thereby resulting in a significant shortening in the effective refractory period at faster rates (0.5 and 0.9 Hz). Results suggest that the "residual fast channel" could produce "slow conduction" and that the ionic channels (fast or slow) responsible for the slow conduction may alternate according to local concentrations of tissue catecholamines.