Inhibition of small-conductance Ca2+-activated K+ channels terminates and protects against atrial fibrillation
Research output: Contribution to journal › Journal article › Research › peer-review
Recently, evidence has emerged that small-conductance Ca(2+)-activated K(+) (SK) channels are predominantly expressed in the atria in a number of species including human. In rat, guinea pig, and rabbit ex vivo and in vivo models of atrial fibrillation (AF), we used 3 different SK channel inhibitors, UCL1684, N-(pyridin-2-yl)-4-(pyridin-2-yl)thiazol-2-amine (ICA), and NS8593, to assess the hypothesis that pharmacological inhibition of SK channels is antiarrhythmic.
| Original language | English |
|---|---|
| Journal | Circulation. Arrhythmia and electrophysiology |
| Volume | 3 |
| Issue number | 4 |
| Pages (from-to) | 380-90 |
| Number of pages | 11 |
| DOIs | |
| Publication status | Published - Aug 2010 |
- 1-Naphthylamine, Acetylcholine, Action Potentials, Alkanes, Animals, Anti-Arrhythmia Agents, Atrial Fibrillation, Cardiac Pacing, Artificial, Dose-Response Relationship, Drug, Electrocardiography, Female, Guinea Pigs, Male, Myocardium, Perfusion, Potassium Channel Blockers, Potassium Channels, Calcium-Activated, Pyridines, Quinolinium Compounds, Rabbits, Rats, Rats, Sprague-Dawley, Thiazoles, Time Factors
Research areas
ID: 33016849