The effect of propranolol and quinidine on 22Na- and 42K-exchange in the cat papillary muscle

Abstract

The present investigation was undertaken to determine if the anti-arrhythmic activity of the β-adrenergic blocking agent, propranolol, is related, at least in part, to a quinidine-like action. For this reason the effect of propranolol was compared to that of quinidine on sodium and potassium fluxes in cat papillary muscle. The actions of propranolol on sodium and potassium exchange were for the most part qualitatively similar to those of quinidine except that propranolol did not affect the total sodium content of papillary muscles. Thus, propranolol like quinidine, caused a decrease in K-efflux, an increase in K-influx and in total potassium content of papillary muscle while it reduced sodium uptake. It did, however, seem to require more propranolol than quinidine to produce these effects. In addition, the action of propranolol on potassium influx and sodium uptake was of shorter duration than that of quinidine. The similarity in the actions of propranolol and quinidine is further indicated by the observation that both of these agents in concentrations which affected potassium and sodium exchange, caused a loss of excitability, i.e., it required a greater intensity of stimulation to cause the muscle to contract in the presence of these agents. The similarity in the effects of quinidine and propranolol on sodium and potassium transmembrane exchange in the present experiments, indicates that the β-adrenergic blocking agent, propranolol, does have the capacity to directly depress cardiac tissue. The role of this action in its anti-arrhythmic effects is discussed.