(1) Cellular Electrophysiology Laboratory, Department of Anesthesia, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA 02115, USA;(2) Department of Biology, State University of New York at Albany, Albany, NY 12222, USA
Abstract:
State-dependent blockade of human cardiac hNav1.5 sodium channels by propafenone was studied using whole-cell patch clamp techniques. Both a direct investigation using cells with inactivation-deficient sodium channels and an algorithmic approach used on cells with wild-type channels revealed a rapid binding of propafenone to the open state. This occurs approximately 4000 and 700 times faster than the binding to the resting and inactivated state, respectively. An established mathematical “gating” model was modified to represent the experimental data.
