内皮素系统与心肌肥厚  

Endothelins system and myocardial hypertrophy

作　　者：孔令雷[1] 颜玲娣[1] 宫泽辉[1] 

机构地区：[1]军事医学科学院毒物药物研究所,北京100850

出　　处：《中国药理学通报》2008年第9期1127-1130,共4页Chinese Pharmacological Bulletin

基　　金：国家高技术研究发展计划(863计划)资助项目(No2006AA020601)

摘　　要：心肌肥厚是心脏对神经介质和压力超负荷等应激反应的一种代偿性机制。内皮素(ET)作为一种具有强大血管收缩作用的活性多肽,在心血管系统,特别是血管内皮细胞、平滑肌细胞和心肌细胞,ET对正常功能的调节起着重要的生理作用。局部心肌组织中ET过度生成与心肌肥厚的发生密切相关,心肌组织中的ET-1通过与特异性的受体结合,并与局部组织中其它相关的血管活性物质相互作用,介导了心肌肥厚的发生和发展过程。内皮素通过ETA受体诱导心肌细胞的肥厚和心肌成纤维细胞的增生,ETB受体则在心肌肥厚的发生和发展中均起作用。内皮素受体作为新的药物靶点,已经成为人们研究的热点,相应的受体拮抗剂的研究也取得了很大的进展。Cardiac hypertrophy is a major adaptational mechanism in stresses sueh as pressure overload and neurohumoral stimulation. As powerful vasoconstrictor peptides in cardiovascular system, especially the vascular endothelium, smooth muscle cells and cardiocyte, ETs play important physiological roles in the regulation of normal cardiovascular function. Excessive generation of ETs in local eardiac muscle has been linked to myocardial hypertrophy. Endothelin-1 （ ET-1 ） in cardiac muscle exerts its actions in the development of myocardial hypertrophy through binding to specific receptors and substance of local tissues. ET-1 cardiocytes and the proliferation interacting with other vasoactive can induce the hypertrophy for for cardiac fibroblasts by ETA. ETB receptors are implicated both in initiating and maintaining myocardial hypertrophy. As a new target of drug, ET receptors have become the research focus, and great progress has been made on the development of the ET antagonists.

关 键 词：内皮素 心肌肥厚 内皮素受体 内皮素受体拮抗剂 

分 类 号：R-05[医药卫生] R349.21