期刊
DIABETES
卷 53, 期 -, 页码 S165-S168出版社
AMER DIABETES ASSOC
DOI: 10.2337/diabetes.53.suppl_3.S165
关键词
-
资金
- NHLBI NIH HHS [HL07111, HL64822] Funding Source: Medline
- NIA NIH HHS [R01 AG021201-02, R01 AG021201, AG21201] Funding Source: Medline
- NIGMS NIH HHS [GM08685] Funding Source: Medline
Metabolic-sensing ATP-sensitive K+ channels (K-ATP channels) adjust membrane excitability to match cellular energetic demand. In the heart, K-ATP channel activity has been linked to homeostatic shortening of the action potential under stress, yet the requirement of channel function in securing cardiac electrical stability is only partially understood. Here, upon catecholamine challenge, disruption of K-ATP channels, by genetic deletion of the pore-forming Kir6.2 subunit, produced defective cardiac action potential shortening, predisposing the myocardium to early afterdepolarizations. This deficit in repolarization reserve, demonstrated in Kir6.2-knockout hearts, translated into a high risk for induction of triggered activity and ventricular dysrhythmia. Thus, intact K-ATP channel function is mandatory for adequate repolarization under sympathetic stress providing electrical tolerance against triggered arrhythmia.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据