Objective: This project, focusing on pharmacological negative modulation of the small conductance Ca2+-activated K+ (SK) channels in the atria of the rat heart, could have the potential of showing a novel path towards treatment of atrial fibrillation (AF). This novel strategy could elucidate SK-channel specific drugs as safer alternatives, minimising the risk of ventricular arrhythmias, due to the abundant expression of SK channels in the atrium of the heart. Methods: The method is a non-pharmacologically induced AF in-vivo model, where short episodes of AF are induced in the rat heart by burst pacing directly on the atrium. This is followed by spontaneous reversion to sinus rhythm. One aim is to quantity the reduction in AF of a negative SK-channel modulator compared to approved antiarrhythmic agents. A number of parameters are monitored during the experiment, used in the analysis of the cardiac action potential electrophysiological modulation (aERP, avERP, BCL, APD etc). Experiments will be conducted in groups of 6 animals. Each group representing a test compound including a placebo group treated with vehicle. This trial will hopefully give significant evidence determining the predictability and clinically relevance of this new model and therapeutic concept. Results: The AF duration is significantly shortened after injection of 5mg/kg NS8593, indicating anti-AF effect of a negative SK-channel modulator. The NS8593(n=7) mediated reduction in AF is 68,5% +-9,5% compared to the vehicle group(n=7). Mean is significantly different from Vehicle (P = 0,0053) Conclusion: These data indicate antiarrhythmic effects of the negative SK-channel modulator (NS8593) in this rat in-vivo model. These findings could reveal SK-channels as a promising new therapeutic target in the treatment of AF with a decreased risk of ventricular proarrhythmia.