Interactions of oxidants with vascular signaling systems

Abstract

Individual reactive oxygen species (ROS) and oxidation products of NO interact with vascular signaling mechanisms in ways that appear to have fundamental roles in the control of vascular physiological and pathophysiological function. The activities of ROS-producing systems (including various NADPH and NADH oxidases, xanthine oxidase, and NO synthase) in endothelium and/or vascular smooth muscle are controlled by receptor activation, oxygen tension, metabolic processes, and physiological forces associated with blood pressure and flow. This review focuses on how the chemical properties and metabolic sensing interactions of individual ROS (including superoxide anion, hydrogen peroxide, and peroxynitrite) interact with cellular regulatory systems to produce vascular responses. These species appear to often function through producing selective alterations in individual heme or thiol redox-regulated systems (including guanylate cyclase, cyclooxygenase, mitochondrial electron transport, and tyrosine phosphatases) to initiate physiological responses through signaling pathways that control phospholipases, protein kinases, ion channels, contractile proteins, and gene expression.