Quinidine Reduces Outward Current in Single Canine Cardiac Purkinje Cells

Abstract

The commonly used antiarrhythmic drug quinidine is a member of the local anesthetic class. In cardiac muscle it reduces sodium (Na) current (1), thereby slowing the action potential (AP) upstroke (2), slowing conduction velocity, and reducing excitability. Quinidine also affects AP repolarization. Typical changes are a prolongation of the AP and a negative shift in the plateau voltage (3), although other studies show either AP shortening (4) or both lengthening and shortening (5). A number of ionic currents contribute to the plateau of the AP, including the inward calcium (Ca) current, slowly inactivating (or “window”) Na current, and three potassium (K) currents: the inward rectifier current, the delayed rectifier, and the transient outward current (I_to). The complex response of the AP to quinidine suggests that it may affect more than one of these repolarizing currents. Effects of drugs on several membrane channels is not rare, but the drug interaction must be to some shared molecular components of the diverse channels. This report addresses the question of quinidine’s effect on I_to in canine cardiac Purkinje cells.