Endothelin-1 and norepinephrine overflow from cardiac sympathetic nerve endings in myocardial ischemia.

Abstract

In protracted myocardial ischemia, sympathetic activation with carrier-mediated excessive norepinephrine (NE) release from its nerve endings due to reversal of NE transporter in an outward direction is a prominent cause of arrhythmias and cardiac dysfunction. Endothelin-1 (ET-1) and its receptors are intimately involved in the regulation of this carrier-mediated NE overflow in protracted myocardial ischemia. The ET-1 system is often complex, sometimes involving opposing actions depending on which receptor subtype is activated, which cells are affected, and whether stimuli are endogenously generated or exogenously applied. Therefore, a detailed understanding of the ET-1 system is important for applying drugs acting on this system in clinical settings for the treatment of ischemic cardiac disease. This article provides a detailed analysis of how the ET-1 system is involved in the regulation of carrier-mediated NE release from sympathetic nerve endings in protracted myocardial ischemia.

• Authors: Masashi Tawa, Satoshi Yamamoto, Mamoru Ohkita, Yasuo Matsumura
• Journal: Cardiology research and practice (Cardiol Res Pract) Vol. 2012 Pg. 789071 ( 2012) ISSN: 2090-0597 [Electronic] United States
• PMID: 22792506 (Publication Type: Journal Article)