Abstract
Emerging evidence has supported a role of inflammation and immunity in the genesis of hypertension. In humans and experimental models of hypertension, cells of the innate and adaptive immune system enter target tissues, including vessels and the kidney, and release powerful mediators including cytokines, matrix metalloproteinases and reactive oxygen species that cause tissue damage, fibrosis and dysfunction. These events augment the blood pressure elevations in hypertension and promote end-organ damage. Factors that activate immune cells include sympathetic outflow, increased sodium within microenvironments where these cells reside, and signals received from the vasculature. In particular, the activated endothelium releases reactive oxygen species and interleukin (IL)-6 which in turn stimulate transformation of monocytes to become antigen presenting cells and produce cytokines like IL-1β and IL-23, which further affect T cell function to produce IL-17A. Genetic deletion or neutralization of these cytokines ameliorates hypertension and end-organ damage. In this review, we will consider in depth features of the hypertensive milieu that lead to these events and consider new treatment approaches to limit the untoward effects of inflammation in hypertension.