AI Article Synopsis
- Voltage activated potassium (Kv) channels, especially the Kv1.5 channel responsible for the IKur current, are being studied as potential drug targets for treating cardiac arrhythmia, particularly atrial fibrillation (AF).
- The inhibition of IKur/Kv1.5 can shorten action potentials in healthy tissue, potentially leading to arrhythmia rather than prevention.
- Chronic AF causes electrical remodeling in tissue, altering ion channel expression and highlighting the need for new strategies to better understand drug interactions and improve treatment outcomes.
Article Abstract
Voltage activated potassium (Kv) channels are intensely investigated targets within the pharmacological strategies to treat cardiac arrhythmia. For atrial fibrillation (AF) substances inhibiting the ultra rapid outward rectifying Kv current (IKur) and its underlying Kv1.5 channel have been developed. Here we describe potential limitations of this approach with respect to critical parameters of Kv channel pharmacology. In healthy tissue IKur/Kv1.5 inhibition can unexpectedly lead to action potential shortening with corresponding arrhythmogenic effects. In tissue with chronic AF, electrical remodeling occurs which is accompanied with changes in ion channel expression and composition. As a consequence atrial tissue exhibits a different pharmacological fingerprint. New strategies to obtain more mechanistic insight into drug target interaction are needed for better understanding the pharmacological potential of IKur/Kv1.5 inhibition for AF treatment.
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| http://dx.doi.org/10.1016/j.coph.2014.02.001 | DOI Listing |
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