Reactive Oxygen Species and Endothelium-Derived Contracting Factor (EDCF) – Partners in Endothelial Dysfunction

Abstract

The augmented release of endothelium-derived contracting factor(s) is a hallmark of endothelial dysfunction. The most common endothelium-derived contracting factors (EDCFs) are produced by endothelial cyclooxygenase(s) and cause activation of thromboxane-prostanoid (TP) receptors of the underlying vascular smooth muscle cells. Endothelium-dependent contractions are exacerbated by aging, endothelial regeneration, hypertension, and diabetes. Elevated oxidative stress and the resulting increased production of reactive oxygen species (ROS) are key aspects of cardiovascular disease and play an important role in the occurrence and/or modulation of endothelium-dependent contraction. This present review summarizes the current knowledge on the interactions between ROS and EDCF in the genesis of endothelial dysfunction in animals and humans as a therapeutic target to restore proper endothelial function and slow down the progression of vascular disease.