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Effect of sotalol on transmembrane ionic currents responsible for repolarization in cardiac ventricular myocytes from
A Varró1, P P Nánási, D A Lathrop
1Department of Pharmacology and Cell Biophysics, University of Cincinnati College of Medicine, Ohio 45276.
Abstract:
The effects of sotalol, a beta-adrenoceptor blocker and class III antiarrhythmic agent, on transmembrane ionic currents were examined in single rabbit and guinea pig ventricular myocytes using whole-cell voltage-clamp techniques. In neither of these species did 60 microM sotalol appreciably effect the inward rectifier, the transient outward or the inward calcium currents. In addition, sotalol did not elicit a slowly inactivating component of the sodium current as did 1 microgram/ml veratrine. In guinea pig ventricular myocytes, sotalol also significantly depressed the outward delayed rectifier current. An outward delayed rectifier current was not observed in rabbit ventricular myocytes examined at room temperature; and, under these conditions sotalol did not lengthen action potential duration. Sotalol induced lengthening of cardiac action potential duration can, therefore, be explained by depression the outward delayed rectifier current.