Effect of metoprolol on sarcoplasmic reticulum Ca^2＋ leak in a rabbit model of heart failure  

作　　者：ZHANG Shi-jie LIU Zhi-hua ZOU Cao WANG Lei 

机构地区：[1]Department of Laboratory MedicineFirst Affiliated Hospital of ZhengzhouUniversity, Zhengzhou, Henan 450052, China [2]Department ofEmergency First Affiliated Hospital of ZhengzhouUniversity, Zhengzhou, Henan 450052, China [3]Department of Cardiology, First Affiliated Hospital of SoochowUniversity, Suzhou, Jiangsu 215006, China

出　　处：《Chinese Medical Journal》2012年第5期815-822,共8页中华医学杂志（英文版）

基　　金：This work was supported in part by grants from the Jiangsu Province ＂135 Project＂ Key Laboratory Fund （No. SK200205） in China and the National Natural Science Foundation of China （No. 30800460）.

摘　　要：Background Studies have shown that B-blockers can improve cardiac performance in heart failure （HF） by reversing protein kinase A （PKA）-mediated sarcoplasmic reticulum （SR） Ca^2＋ leak. However, it is being strongly questioned as to whether the PKA-mediated ryanodine receptor （RyR2） hyper-phosphorylation is a critical regulator of SR Ca^2＋ leak. In this study, we used a rabbit HF model to investigate whether β-blockers affect SR Ca^2＋ leak by other potential mechanisms.Background Studies have shown that B-blockers can improve cardiac performance in heart failure （HF） by reversing protein kinase A （PKA）-mediated sarcoplasmic reticulum （SR） Ca^2＋ leak. However, it is being strongly questioned as to whether the PKA-mediated ryanodine receptor （RyR2） hyper-phosphorylation is a critical regulator of SR Ca^2＋ leak. In this study, we used a rabbit HF model to investigate whether β-blockers affect SR Ca^2＋ leak by other potential mechanisms.

关 键 词：Β-BLOCKER heart failure Ca^2＋ leak ryanodine receptor PHOSPHORYLATION 

分 类 号：Q463[生物学—生理学] Q71