The role of inflammation in hypertension: novel concepts

Abstract

Hypertension remains the most important modifiable risk factor for the development of cardiovascular disease. While it is clear that inflammation plays a pivotal role in the development and maintenance of hypertension, several novel discoveries have been made within the past decade that have advanced the field and have provided new mechanistic insights. First, recent studies have identified a central role of sodium-induced immune cell activation in the pathogenesis of hypertension by altering the gut microbiome and formation of products of lipid oxidation known as isolevuglandins. Second, cytokine elaboration by the inflammasome leading to end-organ dysfunction and immune activation has been found to play a role in the genesis of hypertension. Third, novel techniques have identified previously uncharacterized immune cell populations that may play a functional role in these processes. Finally, the role of inflammation in hypertension may be an important mediator of severe COVID-19 infections. In this review, we discuss these recent advances in the study of inflammation and hypertension and highlight topics for future studies.

Figure 1

Immune activation in hypertension is characterized by activation of dendritic cells (DC) and subsequent activation of T-cells. T-cells then migrate to the vascular tree and the kidney causing inflammation and hypertension. High salt can participate in the activation of immature DCs to activated DCs whereas myeloid derived suppressor cells can inhibit DC and T cell activation. Products of the microbiome and inflammasome both act on innate immune cells and T-cells directly to augment peripheral organ inflammation and exacerbate hypertension. Processes discussed herein are represented by red arrows.