The endothelin receptor antagonist decreases ischemia/reperfusion-induced tumor necrosis factor production in isolated rat hearts.
Previous studies have shown that endothelin-1 (ET-1) may play a pathophysiological role in myocardial ischemia/reperfusion injury. In the present study, BMS-182874 significantly improved the recovery of cardiac function and reduced the release of CK during reperfusion after ischemia and the content of tumor necrosis factor (TNF-alpha) in myocardial tissues. BMS-182874 also reduced myocardial injury and the increased level of TNF-alpha by exogenous ET-1. These results suggest that the cardioprotective effects of the ET receptor antagonist may be related to inhibition of TNF-alpha production.
Yang
Tian-Lun
TL
Chen
Mei-Fang
MF
Jiang
Jun-Ling
JL
Xie
Qi-Ying
QY
Li
Yun-Ping
YP
Li
Yuan-Jian
YJ
D000818:Animals; D000959:Antihypertensive Agents / Q000494:pharmacology*; D003619:Dansyl Compounds / Q000494:pharmacology*; D019332:Endothelin-1 / Q000502:physiology; D066298:In Vitro Techniques; D008297:Male; D015428:Myocardial Reperfusion Injury / Q000378:metabolism*; D009206:Myocardium / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism*
D000959:Antihypertensive Agents; D003619:Dansyl Compounds; D019332:Endothelin-1; D014409:Tumor Necrosis Factor-alpha; C085754:5-(dimethylamino)-N-(3,4-dimethyl-5-isoxazolyl)-1-naphthalenesulfonamide