Pharmacological activation of normal and arrhythmia-associated mutant KCNQ1 potassium channels.

Abstract excerpt

KCNQ1 alpha-subunits coassemble with KCNE1 beta-subunits to form channels that conduct the slow delayed rectifier K+ current (IKs) important for repolarization of the cardiac action potential. Mutations in KCNQ1 reduce IKs and cause long-QT syndrome, a disorder of ventricular repolarization that predisposes affected individuals to arrhythmia and sudden death. Current therapy for long-QT syndrome is inadequate....

Topics

Share this publication in a Topic to start or enrich a Post.

• Share to Anti-Arrhythmia Agents
• Share to Arrhythmias, Cardiac
• Share to Benzodiazepines