Procaine amide reduces the heart rate and alters action potentials in sino-atrial node cells primarily by reducing the outward potassium current.
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Findings in isolated animal SA node cells should not guide clinical use; leaves open iK-mediated mechanisms in intact mammalian hearts.
Using small rabbit sino-atrial node preparations, the effects of procaine amide in concentrations from 0.01 to 2 mg/ml on the membrane potentials currents were studied by both current-clamp and voltage-clamp experiments. Procaine amide in concentrations over 0.1 mg/ml reduced the peak of the action potential, maximum diastolic potential and the maximum rate of depolarization. The action potential duration was prolonged, the resting potential was decreased and the heart rate was reduced. In the voltage-clamp experiments, procaine amide (0.1 mg/ml) reduced the slow inward current (is), the outward current (iK) and the inward current activated by hyperpolarization (ih). The major effect, however, was the reduction of the outward current. Sine the degree of the steady-state activation of iK and its time constant were unchanged, the observed reduction of iK could have been caused by a reduction of iK.
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Senami et al. (1981) studied this question.
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