内皮素1对胞浆Ca^(2+)升高调控作用的研究进展  

Research progress in regulation of endothelin-1 on increase of intracellular Ca^(2+) signaling

作　　者：王涛[1] 肖良[1] 王倩倩[1] 栾湘云[2] 张黎明[1] 

机构地区：[1]第二军医大学海医系防化医学教研室,上海200433 [2]第二军医大学长海医院妇产科,上海200433

出　　处：《中国药理学与毒理学杂志》2012年第4期585-587,共3页Chinese Journal of Pharmacology and Toxicology

基　　金：国家自然科学基金(81000098);国家自然科学基金(41176126)~~

摘　　要：由21个氨基酸残基组成的内皮素1(ET-1)不仅是已知最强的缩血管活性肽,还对血管形成与重构、细胞增殖、细胞外基质合成和感觉神经活化等诸多生理活动具有调控作用。其生理效应多通过升高胞浆Ca2+继而促发连锁反应来实现。增强细胞外Ca2+内流和促进胞内Ca2+释放是ET-1升高胞浆Ca2+浓度的两条基本途径,同时,通过抑制胞内的Ca2+外排与重摄取及对细胞核等非典型Ca2+库内的Ca2+信号的调控同样可以达到升高胞浆Ca2+浓度的目的,本文主要就ET-1升高胞浆Ca2+的调控途径作一综述。The 21-amino-acid peptide endothelin-1 （ET-1） regulates a diverse array of physiological processes, including vasoconstriction, vascular remodeling, angiogenesis, cell proliferation, extracellular matrix synthesis and nociception. Most of the effects of ET-I are associated with an increase in [ Ca^2＋ ] ; （ intracellular calcium concentration）. The increase in [ Ca^2＋ ]; aroused by ET-1 can be due to calcium influx or calcium stores release or a portion of both. In addition, ET-1 also can increase [ Ca^2＋ ] either by decreasing Ca^2＋ efflux, suppressing Ca^2＋ reuptake into sarcoplasmic/endoplasmic reticulum or regulating the Ca^2＋ signal in the nucleus. This paper mainly reviews the regulation of ET-1 on the increase in intracellular Ca^2＋ signalling.

关 键 词：内皮素1 钙信号 肌醇1 4 5-三磷酸受体 兰尼碱受体钙释放通道 

分 类 号：R963[医药卫生—微生物与生化药学]