Inflammation in salt-induced hypertension.

Abstract

Hypertension in the human population became like a worldwide epidemic, increasing risk for cardiovascular diseases. The most important contributor to hypertension among life style factors is high salt intake. Our average intake nowadays exceeds 10 grams per day. In the traditional way, salt increases plasma sodium, which causes a higher blood volume leading to increased blood pressure levels. However, the exact underlying mechanisms of salt, hypertension and salt sensitivity are controversial. Since the last 30 years more attention is focused on the role of inflammation in hypertension. Both the innate and adaptive immune system contribute in hypertension and salt seems to play a role in both immune systems. Salt even affects the communication between them, through antigen presenting cells. Serum glucocorticoid kinase I (SGK-1) links pro-inflammatory T helper 17 cells (Th17) to salt. Th17 cells are activated via SGK-1 by increased concentrations of sodium. T cells can also be activated by neoantigens in salt-induced hypertension, presented by dendritic cells. The contribution of macrophages seems to be the production of reactive oxygen species (ROS). Superoxide reacts with nitric oxide (NO) and decreases availability of NO for vasodilation. Macrophages also contribute in salt storage in the interstitium. The kidney is less able to secrete sodium during inflammation and increased levels of angiotensin II (AngII). AngII could also be originating from immune cells. A high salt diet exacerbates or maintains the inflammatory and hypertensive state. Stiffening of vasculature is directly caused by salt and the activity of immune cells in the Central Nervous System (CNS) seems to react on high sodium concentrations. This thesis provides a new insight in the origin of salt sensitivity, which could be approached as an immunologic disorder.