Effect of procaine amide on the membrane currents of the sino-atrial node cells of rabbits.

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.

[1]  H. Irisawa Comparative physiology of the cardiac pacemaker mechanism. , 1978, Physiological reviews.

[2]  M. Rosen,et al.  Electrophysiologic Properties and Response to Pharmacologic Agents of Fibers from Diseased Human Atria , 1976, Circulation.

[3]  I. Seyama Characteristics of the rectifying properties of the sino‐atrial node cell of the rabbit. , 1976, The Journal of physiology.

[4]  J. Bigger,et al.  The Effect of Procaine Amide on Components of Excitability in Long Mammalian Cardiac Purkinje Fibers , 1976, Circulation research.

[5]  J. Bigger,et al.  Effect of Lidocaine on the Early Inward Transient Current in Sheep Cardiac Purkinje Fibers , 1975, Circulation research.

[6]  M. Rosen,et al.  Electrophysiology and pharmacology of cardiac arrhythmias. VII. Cardiac effects of quinidine and procaine amide. A. , 1975, American heart journal.

[7]  A. Noma,et al.  The effect of sodium ion on the initial phase of the sinoatrial pacemaker action potentials in rabbits. , 1974, The Japanese journal of physiology.

[8]  B. Singh,et al.  Comparative mechanisms of action of antiarrhythmic drugs. , 1974, American heart journal.

[9]  M. Rosen,et al.  Effects of procaine amide on the electrophysiologic properties of the canine ventricular conducting system. , 1973, The Journal of pharmacology and experimental therapeutics.

[10]  M. Rosen,et al.  Mechanisms of Action of Antiarrhythmic Drugs , 1973, Circulation research.

[11]  M. Rosen,et al.  Canine Electrocardiographic and Cardiac Electrophysiologic Changes Induced by Procainamide , 1972, Circulation.

[12]  D. Noble,et al.  Outward membrane currents activated in the plateau range of potentials in cardiac Purkinje fibres , 1969, The Journal of physiology.

[13]  D. Noble,et al.  Reconstruction of the repolarization process in cardiac Purkinje fibres based on voltage clamp measurements of membrane current , 1969, The Journal of physiology.

[14]  D. Noble,et al.  The kinetics and rectifier properties of the slow potassium current in cardiac Purkinje fibres , 1968, The Journal of physiology.

[15]  S. Weidmann,et al.  The effect of the cardiac membrane potential on the rapid availability of the sodium‐carrying system , 1955, The Journal of physiology.

[16]  C. Brooks,et al.  The effect of procaine amide on excitability, refractoriness and conduction in the mammalian heart. , 1953, The Journal of pharmacology and experimental therapeutics.