Adrenaline and the plateau phase of the cardiac action potential

Summary

Conduction block in heart cells by K⁺ rich, or Na⁺ depleted solutions can be overcome by adrenaline. In order to explain this phenomenon, the effect of adrenaline on the membrane resting and action potentials of cow Purkinje fibers was measured at various extracellular concentrations of Na⁺, K⁺ and Ca⁺⁺, in the presence of tetrodotoxin, Mn⁺⁺ and beta-receptor antagonists.

It was found that adrenaline specifically increases the amplitude and duration of the plateau phase of the cardiac action potential. Plateu-like action potentials, without preceding Na⁺-spike, can be generated and conducted in an all-or-nothing way. In K⁺ rich solutions and under the influence of adrenaline, the depolarization proceeds in two steps. The first step corresponds to the Na⁺-spike. The second step or secondary depolarization corresponds to the plateau; it was not modified by changes of the membrane potential between −85 and −55 mV, or by reduction of extracellular Na⁺ ions, but was specifically blocked by Mn⁺⁺ ions and beta-receptor antagonists. Its amplitude increased by 17 mV for a tenfold change in extracellular Ca⁺⁺. Tetrodotoxin preferentially blocked the Na⁺-spike, but also slowed the rate of potential change during the secondary depolarization.

The simplest explanation for the observed phenomena can be found in an increase of Ca⁺⁺ inward current under the influence of adrenaline. The existence of an inward Na⁺⁺ current, different in characteristics from the Na⁺ conductance during the fast upstroke, cannot be ruled out. Some data are in accord with a decrease in K⁺ conductance.