The endothelin receptor antagonist decreases ischemia/reperfusion-induced tumor necrosis factor production in isolated rat hearts.

Abstract

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.

• Authors: Tian-Lun Yang, Mei-Fang Chen, Jun-Ling Jiang, Qi-Ying Xie, Yun-Ping Li, Yuan-Jian Li
• Journal: International journal of cardiology (Int J Cardiol) Vol. 100 Issue 3 Pg. 495-8 (Apr 28 2005) ISSN: 0167-5273 [Print] Netherlands
• PMID: 15837096 (Publication Type: Letter)

Chemical References

• Antihypertensive Agents
• Dansyl Compounds
• Endothelin-1
• Tumor Necrosis Factor-alpha
• 5-(dimethylamino)-N-(3,4-dimethyl-5-isoxazolyl)-1-naphthalenesulfonamide

Topics

• Animals
• Antihypertensive Agents (pharmacology)
• Dansyl Compounds (pharmacology)
• Endothelin-1 (physiology)
• In Vitro Techniques
• Male
• Myocardial Reperfusion Injury (metabolism)
• Myocardium (metabolism)
• Rats
• Rats, Sprague-Dawley
• Tumor Necrosis Factor-alpha (metabolism)