Pharmacological activation of rapid delayed rectifier potassium current suppresses bradycardia-induced triggered activity in the isolated guinea pig heart.

@article{Hansen2007PharmacologicalAO,
  title={Pharmacological activation of rapid delayed rectifier potassium current suppresses bradycardia-induced triggered activity in the isolated guinea pig heart.},
  author={Rie Schultz Hansen and S. -P. Olesen and Morten Grunnet},
  journal={The Journal of pharmacology and experimental therapeutics},
  year={2007},
  volume={321 3},
  pages={996-1002}
}
Recently, attention has been drawn to compounds that activate the human ether-a-go-go channel potassium channel (hERG), which is responsible for the repolarizing rapid delayed rectifier potassium current (I(Kr)) in the mammalian myocardium. The compound NS3623 [N-(4-bromo-2-(1H-tetrazol-5-yl)-phenyl)-N'-(3'-trifluoromethylphenyl) urea] increases the macroscopic current conducted by the hERG channels by increasing the time constant for channel inactivation, which we have reported earlier. In… CONTINUE READING

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