Salt Intake and Immunity

Increased salt intake has been associated with cardiovascular disease,1 and it has been suggested that reductions in dietary salt could substantially reduce cardiovascular events and medical costs and, therefore, should be a public health target.2 The relationship between salt intake and cardiovascular diseases involves the complex interplay of several factors that include age, sex, the renin–angiotensin–aldosterone and kallikrein–kinin systems, sympathetic nervous system activity, endothelial function, and redox balance.3 In addition, it is now recognized that the immune system plays an active role in the development and progression of hypertension, and salt intake not only drives hemodynamic changes but is also associated with changes in the immune responses. Here we review the evidence that indicates that salt intake modulates immune function and salt-driven proinflammatory reactivity induces vascular endothelial dysfunction, immune cell activation, and cytokine secretion, all of which are central characteristics of hypertensive cardiovascular disease. Endothelial dysfunction is one of the central characteristics of hypertension and is associated with overexpression of leukocyte adhesion molecules and local inflammation. In spontaneously hypertensive rats, overexpression of ICAM-1 (intercellular adhesion molecule-1), MCP-1 (monocyte chemotactic protein-1), and macrophage adhesion ligand-1 (a cell-surface protein expressed in most leukocytes) has been demonstrated in association with increased monocyte endothelial adhesiveness. These findings play a role in end-organ damage.4–7 Takahashi et al4 studied changes in leukocyte adhesiveness induced by sodium intake in Dahl salt–sensitive rats. They examined adhesion of leukocytes to retinal vessels using acridine orange fluoroscopy and scanning laser ophthalmoscope and followed the expression of adhesion molecules in the kidney. After only 3 days of a diet with 8% NaCl, before hypertension developed, leukocyte adhesion was increased in association with increments in mRNA synthesis of MCP-1 and ICAM-1 in the kidney. Anti-CD18 antibodies inhibited these early effects of high salt intake and …