May 15, 2009Circulation ResearchOpen Access

Antiarrhythmic Drug-Induced Internalization of the Atrial-Specific K+Channel Kv1.5

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Population

HL-1 atrial myocytes expressing Kv1.5-GFP and acutely dissociated neonatal myocytes

Design

Preclinical

Authors

SSSarah M. SchumacherCleveland Clinic DMDyke P. McEwenUniversity of Michigan LZLian ZhangArmy Medical University

Discussion

Member takes

Implication

Quinidine may induce Kv1.5 degradation beyond pore block; animal findings leave open translation to human antiarrhythmic therapy.

Structured PICO

Population

HL-1 atrial myocytes expressing Kv1.5-GFP and acutely dissociated neonatal myocytes

Intervention

Quinidine (class I antiarrhythmic agent), acute and chronic treatment

Outcome

Internalization of Kv1.5 and channel blocksurrogate

Quinidine induces calcium-dependent internalization and degradation of the atrial-specific Kv1.5 channel, revealing a novel mechanism of antiarrhythmic drug action beyond simple pore block.

Cite This Study

Schumacher et al. (2009) studied this question.

synapsesocial.com/papers/6a20798e14cb6ef00ff48d35 https://doi.org/10.1161/circresaha.108.192773

Topics

Persistent AF management Atrial fibrillation

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Antiarrhythmic Drug-Induced Internalization of the Atrial-Specific K+Channel Kv1.5

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Topics

Antiarrhythmic Drug-Induced Internalization of the Atrial-Specific K+Channel Kv1.5

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Topics

Also Consider