Inflammation in Hypertension

Abstract

For more than 50 years, evidence has accumulated that inflammation contributes to the pathogenesis of hypertension. Immune cells have been observed in vessels and kidneys of hypertensive humans. Biomarkers of inflammation, including high sensitivity C-reactive protein, various cytokines, and products of the complement pathway are elevated in humans with hypertension. Emerging evidence suggests that hypertension is accompanied and indeed initiated by activation of complement, the inflammasome, and by a change in the phenotype of circulating immune cells, particularly myeloid cells. High-dimensional transcriptomic analyses are providing insight into new subclasses of immune cells that are likely injurious in hypertension. These inflammatory events are interdependent and there is ultimately engagement of the adaptive immune system through mechanisms involving oxidative stress, modification of endogenous proteins, and alterations in antigen processing and presentation. These observations suggest new therapeutic opportunities to reduce end organ damage in hypertension might be used and guided by levels of inflammatory biomarkers.