Block and modulation of cardiac Na+ channels by antiarrhythmic drugs, neurotransmitters and hormones.
The Na+ channel is an important target for the action of antiarrhythmic drugs. Application of contemporary biophysical, biochemical and molecular biological techniques have added considerably to our knowledge of its structure, function, modulation and block by antiarrhythmic drugs. The increased mortality from the use of these drugs for prophylaxis of cardiac arrhythmias has forced a re-evaluation of their use and of the entire pharmacological strategy of arrhythmia management. Gus Grant and David Wendt review recent studies on the block and modulation of cardiac Na+ channels and the place of Na+ channel blockers in future antiarrhythmic drug development.
Grant
A O
AO
Department of Medicine, Duke University Medical Center, Durham, NC 27706.
Wendt
D J
DJ
D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000494:pharmacology*; D001667:Binding, Competitive; D006321:Heart / Q000187:drug effects*; D006728:Hormones / Q000494:pharmacology*; D009206:Myocardium / Q000378:metabolism; D018377:Neurotransmitter Agents / Q000494:pharmacology*; D015222:Sodium Channels / Q000187:drug effects*; D013329:Structure-Activity Relationship
D000889:Anti-Arrhythmia Agents; D006728:Hormones; D018377:Neurotransmitter Agents; D015222:Sodium Channels