Population
Newborn mice and their ventricular myocytes with targeted deletion of Kir2.1 and Kir2.2 genes
Comparison
Targeted deletion of Kir2.1 and Kir2.2 genes vs Wild-type mice and myocytes
Design
Preclinical
Key result
Targeted deletion of Kir2.1 in murine ventricular myocytes eliminated detectable I(K1), resulting in broader action potentials and increased automaticity without causing re-entry arrhythmias.
Authors
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Does not inform clinical arrhythmia management; leaves open Kir2.1's role in human ventricular electrophysiology.
Kir2.1 is the major component of the murine I(K1) current, and its deletion prolongs action potentials and slows heart rate without inducing severe arrhythmias in neonates.
Zaritsky et al. (2001) studied Cardiac inwardly rectifying K+ current (I(K1)) disruption. Targeted deletion of Kir2.1 and Kir2.2 genes vs. Wild-type mice was evaluated on I(K1) current and action potential characteristics. Targeted deletion of Kir2.1 in murine ventricular myocytes eliminated detectable I(K1), resulting in broader action potentials and increased automaticity without causing re-entry arrhythmias.