ABSTRACT
Oxidative stress and low-grade subclinical chronic inflammation are interdependent processes that play an important role in pathophysiological mechanisms underlying hypertension (HTN). Inflammatory cells release reactive oxygen species (ROS) at the site of inflammation increasing oxidative stress, which promotes oxidative injury and cell death. ROS play a critical role in mediating intracellular redox-dependent signalling, further influencing inflammation through stimulatory effects on transcription factors inducing proinflammatory gene expression. The relationship between ROS, immune cells and HTN is complex because ROS are important mediators of immune cell function while at the same time are also activators of the immune system in HTN. Both innate and adaptive immune systems may contribute to the pathogenesis of cardiovascular disease, vascular remodelling and HTN Almost every cell type involved in innate and adaptive immunity has been suggested to be involved in the pathophysiology of HTN. Enhanced adaptive immunity arising from a genetic predisposition may underlie vascular inflammation.
