Inhibition of small-conductance Ca2+-activated K+ channels terminates and protects against atrial fibrillation

Jonas Goldin Diness, Ulrik S Sørensen, Jakob Dahl Nissen, Baha Al-Shahib, Thomas Jespersen, Morten Grunnet, Rie Schultz Hansen, Thomas Jespersen

Research output: Contribution to journalJournal articleResearchpeer-review

166 Citations (Scopus)

Abstract

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 languageEnglish
JournalCirculation. Arrhythmia and electrophysiology
Volume3
Issue number4
Pages (from-to)380-90
Number of pages11
DOIs
Publication statusPublished - Aug 2010

Keywords

  • 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

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