EFFECT OF PROPRANOLOL ON THE FAST INWARD SODIUM CURRENT IN FROG ATRIAL MUSCLE

¹ Department of Physiology, University of Kansas Medical Center, Kansas City, Kansas, and First Physiologisches Institut der Universität Heidelberg, Germany
² Department of Physiology, University of Kansas Medical Center, Kansas City, Kansas, and First Physiologisches, Institut der Universität Heidelberg, Germany

The purpose of this investigation was to deterimine the effect of dl-propranolol, l-propranolol and d-propranolol on the inward sodium current responsible for the rapid depolarization phase of the cardiac action potential. This was accomplished by the use of the double sucrose-gap voltage clamp techinique on frog atrial muscle fibers. Each drug at a concentration of 10^-5g/ml suppressed the maximum magnitude of the inward sodium current (I_max) by approximately 50%. The reduction in the sodium current was associated with a proportional reduction in the maximum transient conductance (g_p). Propranolol shifted the steady-state inactivation curve 4 mV toward more negative membrane potentials but the decrease (about 5%) in the magnitude of the inactivation variable (h) at the normal resting potential was not sufficient to account for the reduction in either I_max or g_p. The rate of inactivation of the inward sodium current was not affected by propranolol and there did not appear to be any significant alteration in the rate of activation of the sodium current. In contrast, the rate of reactivation of the sodium current was sometimes prolonged by propranolol. which accounted for a prolongation of the effective refractory period. The data demonstrate that propranolol suppresses the inward sodium current by blocking the sodium channels, thereby causing a reduction in the maximum sodium conductance (g_Na).