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Abstract
Summary: The effects of recainam (Wy 42,362) on transmembrane action potentials were examined in isolated rabbit right ventricular papillary muscles. Recainam (3 × 10−5 to 3 × 10−4M) caused a concentration-dependent decrease in the JOURNAL/jcph/04.03/00005344-198904000-00017/OV0312/v/2021-02-06T190858Z/r/image-pngmax of the action potential. At 3 × 10−4M, there was a slight decrease in the amplitude of the action potential. The resting potential and the action potential duration were not affected. Use-dependent block of JOURNAL/jcph/04.03/00005344-198904000-00017/OV0312/v/2021-02-06T190858Z/r/image-pngmax was tested over a wide range of pacing frequencies (from 0.1 to 3.0 Hz). At 1.0 Hz, recainam 10−4M produced exponential decreases in JOURNAL/jcph/04.03/00005344-198904000-00017/OV0312/v/2021-02-06T190858Z/r/image-pngmax with a rate constant of 0.17 per action potential and 39.8% reduction at steady state. This use-dependent block was augmented at the higher stimulation frequencies. The time constant for the recovery of JOURNAL/jcph/04.03/00005344-198904000-00017/OV0312/v/2021-02-06T190858Z/r/image-pngmax from use-dependent block (offset) was 17.2 s. In papillary muscles depolarized with 10 mM [K+]0, the use-dependent block was augmented but tonic block and the rates of onset and offset of the use-dependent block were similar to those in normally polarized preparations in 4 mM [K+]0. The curves relating membrane potential and JOURNAL/jcph/04.03/00005344-198904000-00017/OV0312/v/2021-02-06T190858Z/r/image-pngmax in preparations stimulated at a low frequency (0.01 Hz) were not shifted by 10−4M recainam. These findings suggest that recainam is a specific sodium-channel blocker and has kinetically slow but potent affinity for the channel during action potentials. This selective binding during action potential was further augmented by depolarization and is likely to play a significant role in the control of ventricular arrhythmias by the drug.
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