The ET axis mediates arrhythmogenesis and compromised cardiac function in two cardiomyopathy models  

作　　者：YuFENG De-zaiDAI YuanZHANG Hai-boHE Min-youQI YinDAI FengYU 

机构地区：[1]ResearchDivisionofPharmacology,ChinaPharmaceuticalUniversity,Nanjing210009

出　　处：《中国药理通讯》2005年第2期29-30,共2页

摘　　要：AIM Endothelin 1(ET-1), a potent vasoconstrictor peptide, is also regarded as an important etiological factor involved in many cardiac diseases like heart failure and cardiac hypertrophy. It mediates pathologic changes by forming an """"ET axis"""" at the upstream to ion channels, such as stimulating oxidant stress, eliciting cardiac remodeling by proliferation of cardiomyocytes, inducing apoptosis, affecting signal transduction pathway, and modulating intranuclear gene transcription. The purpose of this study was to investigate the pivotal role by ET axis in worsening arrhythmias and cardiac function in experimental hypertrophic cardiomyopathy (HCM) and heart failure (HF) models. METHODS The rat HCM model was induced by s.c L-thyroxin (L-thy, 0.2mg/Kg/d) for 10d,

关 键 词：ET轴 调节作用 节律运动障碍 强心剂 心肌症 动物模型 ET-1 血管收缩 

分 类 号：R542.2[医药卫生—心血管疾病]