Vascular Smooth Muscle Modulates Endothelial Control of Vasoreactivity via Reactive Oxygen Species Production through Myoendothelial Communications

Abstract

These data demonstrate that agonist-induced ROS production in SMC targeting EC via myoendothelial gap junctions reduces endothelial NO-dependent control of pulmonary vasoreactivity. Such SMC modulation of endothelial control may represent a signaling pathway controlling vasoreactivity under not only physiological but also pathological conditions that often implicate excessive ROS production.