Do high-salt microenvironments drive hypertensive inflammation?

Abstract

Hypertension is a global epidemic affecting over one billion people worldwide. Despite this, the etiology of most cases of human hypertension remains obscure, and treatment remains suboptimal. Excessive dietary salt and inflammation are known contributors to the pathogenesis of this disease. Recently, it has been recognized that salt can accumulate in the skin and skeletal muscle, producing concentrations of sodium greater than the plasma in hypertensive animals and humans. Such elevated levels of sodium have been shown to alter immune cell function. Here, we propose a model in which tissue salt accumulation causes an immune response leading to renal and vascular inflammation and hypertension.

Keywords: hypertension; inflammation; salt.

Fig. 1.

Paradigm illustrating how salt may affect immune cells to promote hypertension. High salt drives T cells toward a prohypertensive IL-17 phenotype, both directly and indirectly through activation of antigen-presenting cells (APC), such as monocytes, macrophages, and dendritic cells. This T-cell activation leads to renal and vascular inflammation, dysfunction of the kidneys and vasculature, and ultimately hypertension.