| Autor: |
Patik JC; Department of Kinesiology and Applied Physiology, University of Delaware, 540 S College Ave., Newark, DE 19713, USA., Lennon SL; Department of Kinesiology and Applied Physiology, University of Delaware, 540 S College Ave., Newark, DE 19713, USA., Farquhar WB; Department of Kinesiology and Applied Physiology, University of Delaware, 540 S College Ave., Newark, DE 19713, USA., Edwards DG; Department of Kinesiology and Applied Physiology, University of Delaware, 540 S College Ave., Newark, DE 19713, USA. |
| Abstrakt: |
Despite decades of efforts to reduce sodium intake, excess dietary sodium remains commonplace, and contributes to increased cardiovascular morbidity and mortality independent of its effects on blood pressure. An increasing amount of research suggests that high-sodium diets lead to reduced nitric oxide-mediated endothelial function, even in the absence of a change in blood pressure. As endothelial dysfunction is an early step in the progression of cardiovascular diseases, the endothelium presents a target for interventions aimed at reducing the impact of excess dietary sodium. In this review, we briefly define endothelial function and present the literature demonstrating that excess dietary sodium results in impaired endothelial function. We then discuss the mechanisms through which sodium impairs the endothelium, including increased reactive oxygen species, decreased intrinsic antioxidant defenses, endothelial cell stiffening, and damage to the endothelial glycocalyx. Finally, we present selected research findings suggesting that aerobic exercise or increased intake of dietary potassium may counteract the deleterious vascular effects of a high-sodium diet. |
