State-dependent block of human cardiac hNav1.5 sodium channels by propafenone.
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.
Edrich
T
T
Cellular Electrophysiology Laboratory, Department of Anesthesia, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA. tedrich@partners.org
Wang
S-Y
SY
Wang
G K
GK
D000889:Anti-Arrhythmia Agents / Q000494:pharmacology*; D002460:Cell Line; D006321:Heart / Q000187:drug effects* / Q000502:physiology; D006801:Humans; D007700:Kinetics; D008954:Models, Biological; D009124:Muscle Proteins / Q000037:antagonists & inhibitors* / Q000235:genetics / Q000502:physiology; D016297:Mutagenesis, Site-Directed; D062554:NAV1.5 Voltage-Gated Sodium Channel; D018408:Patch-Clamp Techniques; D011405:Propafenone / Q000494:pharmacology*; D026941:Sodium Channel Blockers / Q000494:pharmacology*; D015222:Sodium Channels / Q000235:genetics / Q000502:physiology
D000889:Anti-Arrhythmia Agents; D009124:Muscle Proteins; D062554:NAV1.5 Voltage-Gated Sodium Channel; C568320:SCN5A protein, human; D026941:Sodium Channel Blockers; D015222:Sodium Channels; D011405:Propafenone