Abstract
The effects of micromolar concentrations of racemic D600 on the transmembrane inward sodium current (INa) were investigated in voltage clamped, intracellularly perfused, human heart cell segments. Extracellular D600 blocked INa in a 'voltage- and rate-dependent' manner as shown by the enhanced INa depression with a reduction of the 'resting' transmembrane polarization (Vmo) and stimulation interval (SI). D600 action was manifested as a voltage-dependent slowing down of the Na+ channels' recovery kinetics after a pulsed excitation, with greater recovery times during longer depolarized states, excited or non-excited. This phenomenon seems linked to the improved control of the intracellular environment normally influencing channel activity, and to the increased ratio of 'non-sarcolemmal' to 'sarcolemmal' cell membranes for this preparation.
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