Bisoprolol reverses down-regulation of potassium channel proteins in ventricular tissues of rabbits with heart failure  

作　　者：Xi Li Tingzhong Wang Ke Han Xiaozhen Zhuo Qun Lu Aiqun Ma 

机构地区：[1]Department of Cardiovascular Medicine, the First Affiliated Hospital of Medical School, Xi＇an Jiaotong University, Xi ＇an, Shaanxi 710061, China [2]Key Laboratory of Molecular Cardiology of Shaanxi Province, Xi ＇an, Shaanxi 710061, China [3]Key Laboratory of Enwronment and Genes Related to Diseases, Xi＇an Jiaotong University, Xi＇an, Shaanxi 710061, China [4]Department of Cardiovascular Medicine, the Second Affiliated Hospital of Medical School, Ningxia Medical University, Yinehuan, Ningxia Hui Autonomous Region 750001, China

出　　处：《The Journal of Biomedical Research》2011年第4期274-279,共6页生物医学研究杂志（英文版）

基　　金：supported by the State Key Program of the National Natural Science Foundation of China (No. 30830051)

摘　　要：Remodeling of ion channels is an important mechanism of arrhythmia induced by heart failure （HF）. We investigated the expression of potassium channel encoding genes in the ventricles of rabbit established by volumeoverload operation followed with pressure-overload. The reversible effect of these changes with bisoprolol was also evaluated. The HF group exhibited left ventricular enlargement, systolic dysfunction, prolongation of corrected QT interval （QTc）, and increased plasma brain natriuretic peptide levels in the HF rabbits. Several potassium channel subunit encoding genes were consistently down-regulated in the HF rabbits. After bisoprolol treatment, heart function was improved significantly and QTc was shortened. Additionally, the mRNA expression of potassium channel subunit genes could be partially reversed. The down-regulated expression of potassium channel subunits Kv4.3, Kv1.4, KvLQT1, minK and Kir 2.1 may contribute to the prolongation of action potential duration in the heart of rabbits induced by volume combined with pressure overload HF. Bisoprolol could partially reverse these down-regulations and improve heart function.Remodeling of ion channels is an important mechanism of arrhythmia induced by heart failure （HF）. We investigated the expression of potassium channel encoding genes in the ventricles of rabbit established by volumeoverload operation followed with pressure-overload. The reversible effect of these changes with bisoprolol was also evaluated. The HF group exhibited left ventricular enlargement, systolic dysfunction, prolongation of corrected QT interval （QTc）, and increased plasma brain natriuretic peptide levels in the HF rabbits. Several potassium channel subunit encoding genes were consistently down-regulated in the HF rabbits. After bisoprolol treatment, heart function was improved significantly and QTc was shortened. Additionally, the mRNA expression of potassium channel subunit genes could be partially reversed. The down-regulated expression of potassium channel subunits Kv4.3, Kv1.4, KvLQT1, minK and Kir 2.1 may contribute to the prolongation of action potential duration in the heart of rabbits induced by volume combined with pressure overload HF. Bisoprolol could partially reverse these down-regulations and improve heart function.

关 键 词：heart failure potassium channel DOWN-REGULATION animal models 

分 类 号：Q73[生物学—分子生物学] Q463