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Effects of MS‐551, a new class III antiarrhythmic drug, on action potential and membrane currents in rabbit ventricular myocytes
Author(s) -
Nakaya Haruaki,
Tohse Noritsugu,
Takeda Youji,
Kanno Morio
Publication year - 1993
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1993.tb13546.x
Subject(s) - sotalol , depolarization , electrophysiology , inward rectifier potassium ion channel , chemistry , membrane potential , effective refractory period , anti arrhythmia agents , refractory period , repolarization , pharmacology , medicine , cardiac transient outward potassium current , antiarrhythmic agent , potassium channel , potassium channel blocker , patch clamp , ion channel , biochemistry , heart disease , receptor , atrial fibrillation
1 Electrophysiological effects of MS‐551, a new class III antiarrhythmic drug, were examined and compared with those of (+)‐sotalol in rabbit ventricular cells. 2 In rabbit ventricular muscles stimulated at 1.0 Hz, MS‐551 (0.1–10 μ m ) and (+)‐sotalol (3–100 μ m ) prolonged action potential duration (APD) and effective refractory period without affecting the maximum upstroke velocity of phase 0 depolarization . The class III effect of MS‐551 was approximately 30 times more potent than that of (+)‐sotalol. 3 Class III effects of MS‐551 and (+)‐sotalol showed reverse use‐dependence, i.e., a greater prolongation of APD at a longer cycle length. 4 In rabbit isolated ventricular cells, 3 μ m MS‐551 and 100 μ m sotalol inhibited the delayed rectifier potassium current ( I K ) which was activated at more positive potentials than −50 mV and saturated around + 20 mV. 5 MS‐551 at a higher concentration of 10 μ m decreased the transient outward current ( I to ) and the inward rectifier potassium current ( I K1 ) although 100 μ m sotalol failed to inhibit these currents. 6 MS‐551 is a non‐specific class III drug which can inhibit three voltage‐gated K + channels in rabbit ventricular cells.