ABSTRACT
Inflammatory events in hypertension have been proposed for many years. Recent data suggest that inflammation causes vascular oxidative stress through stimulation of reactive oxygen species (ROS) production by leukocytes and vascular wall cells. The increased ROS change protein function and gene expression leading to activation of other inflammatory events including adhesion molecule and cytokine expression, recruitment and activation of leukocytes and vascular cells. Inflammation also causes endothelial dysfunction through either direct interaction between inflammatory cytokines and endothelial cells, or indirectly through increased oxidative stress. Finally changes in vascular wall structure and function ensue mediated by vascular smooth muscle cell (VSMC) proliferation establishing hypertension and augmenting cardiovascular disease (Figure 35.1).
