Endothelin (ET) is a family of potent vasoconstrictive peptides mainly distributed in the cardiovascular system. ET 1, the primary isoform of ET in the cardiovascular system, is produced by endothelial cells, cardiomyocytes and smooth muscle cells. Exogenous ET 1 was shown to not only result in myocardial ischemia and arrhythmia via coronary constriction, but also to have pro ischemic and pro arrhythmogenic effects. Endogenous ET 1 is involved in myocardial ischemia/hypoxia. It has been reported that short time ischemia no longer than several minutes could cause release of ET 1 from ischemic myocardium, and longer time ischemia up regulation of ET 1 biosynthesis in ischemic myocardium. Similar to the effects of exogenous ET 1, increased endogenous ET 1 during ischemia tend to aggravate myocardial ischemia via coronary constriction, and exert pro ischemic and pro arrhythmogenic effects as well. It possibly contributes to the genesis of ischemic arrhythmia. This article chiefly reviewed the studies on exogenous ET 1 and arrhythmia, and endogenous ET 1 in ischemic arrhythmia.
