Targeted Replacement of Kv1.5 in the Mouse Leads to Loss of the 4-Aminopyridine–Sensitive Component of I K,slow and Resistance to Drug-Induced QT Prolongation

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Population

Mice (homozygous SWAP mice with mKv1.5 replaced by rKv1.1 and littermate controls)

Comparison

Gene targeting to replace mKv1.5 with the… vs Littermate controls

Design

Preclinical

Authors

Discussion

Supports Kv1.5 mediation of 4-AP-sensitive repolarization in mice; leaves open translation to human arrhythmia mechanisms.

Population

Mice (homozygous SWAP mice with mKv1.5 replaced by rKv1.1 and littermate controls)

Intervention

Gene targeting to replace mKv1.5 with the 4-aminopyridine (4-AP)-insensitive channel rKv1.1 (SWAP mice)

Comparator

Littermate controls

Outcome

Electrophysiological properties including I(K,slow) density, APD90, and QTc prolongation in response to 4-aminopyridine (4-AP)surrogate

Kv1.5 encodes the 4-AP-sensitive component of I(K,slow) in the mouse ventricle and confers sensitivity to 4-AP-induced QTc prolongation.

London et al. (2001) studied this question.

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