Lidocaine blocks Na, Ca and K currents of chick ventricular myocytes.
In addition to the well-known reduction in the maximal rate of rise the antiarrhythmic agent, lidocaine, also produces a shortening in the duration of the normal ventricular action potential. The voltage-dependent currents carried by Na, Ca and K ions were examined in the absence and presence of lidocaine, in order to identify the ionic mechanism(s) underlying the action potential shortening. Whole-cell and single channel currents were studied by the patch clamp method using single ventricular myocytes from embryonic chick hearts. Exposure to lidocaine (10 to 1000 microM) produced a decrease in the magnitude of the small-magnitude, slowly-inactivating component of the Na current, and a decrease in the magnitude of the Ca current; these results provide a mechanism for the action potential shortening and suggest possible explanations for the antiarrhythmic action of this therapeutic agent. A decrease in the magnitude of the inwardly-rectifying K+ current was also found, which was attributable to a reduction in the probability of opening of single K+ channels.
Josephson
I R
IR
Department of Physiology and Biophysics, Wright State University, Dayton, Ohio 45267.
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D002118:Calcium / Q000502:physiology*; D002478:Cells, Cultured; D002642:Chick Embryo; D006352:Heart Ventricles / Q000166:cytology / Q000187:drug effects; D007473:Ion Channels / Q000187:drug effects / Q000502:physiology; D008012:Lidocaine / Q000494:pharmacology*; D011188:Potassium / Q000502:physiology*; D012964:Sodium / Q000502:physiology*; D013779:Tetrodotoxin / Q000494:pharmacology; D016276:Ventricular Function
D007473:Ion Channels; D013779:Tetrodotoxin; D008012:Lidocaine; D012964:Sodium; D011188:Potassium; D002118:Calcium