Vascular effects of dietary salt

Abstract

Purpose of review: High dietary salt intake is detrimental in hypertensive and salt-sensitive individuals; however, there are a large number of normotensive salt-resistant individuals for whom dietary salt may also be harmful as a result of the blood pressure-independent effects of salt. This review will focus on the growing evidence that salt has adverse effects on the vasculature, independent of blood pressure.

Recent findings: Data from both animal and human studies provide evidence that salt impairs endothelial function and increases arterial stiffness, independent of blood pressure. High dietary salt results in oxidative stress and increased endothelial cell stiffness, which impair endothelial function, whereas transforming growth factor beta promotes increased arterial stiffness in the presence of endothelial dysfunction.

Summary: Health policies and most clinical research are focused on the adverse effects of dietary salt on blood pressure; however, there is an increasing body of evidence to support a deleterious effect of dietary salt on endothelial function and arterial stiffness independent of blood pressure. Endothelial dysfunction and increased arterial stiffness are predictors of cardiovascular disease; therefore, reducing excess dietary salt should be considered important for overall vascular health in addition to blood pressure.

Figure 1

Proposed mechanisms by which high salt intake leads to reduced nitric oxide (NO) bioavailablilty. High salt leads to increased superoxide (O₂^-) production and suppression of angiotensin II (Ang II) which leads to decreased superoxide dismutase (SOD) expression and activity reducing scavenging of O₂^-. NO bioavailability is decreased by the following: 1) via reaction of NO with O₂^- to form peroxynitrite (OONO^-); 2) oxidation of endothelial nitric oxide synthase (eNOS) cofactor tetrahydrobiopterin (BH₄) reducing NO synthesis; and 3) an increase in endothelial cell stiffness which leads to decreased synthesis of NO.