Mechanisms and consequences of salt sensitivity and dietary salt intake

Purpose of review Investigation into the underlying mechanisms of salt sensitivity has made important advances in recent years. This review examines in particular the effects of sodium and potassium on vascular function. Recent findings Sodium chloride (salt) intake promotes cutaneous lymphangiogenesis mediated through tissue macrophages and directly alters endothelial cell function, promoting increased production of transforming growth factor-beta (TGF-beta) and nitric oxide. In the setting of endothelial dysfunction, such as occurs with aging, diminished nitric oxide production exacerbates the vascular effects of TGF-beta, promoting decreased arterial compliance and hypertension. Dietary potassium intake may serve as an important countervailing influence on the effects of salt in the vasculature. Summary There is growing appreciation that, independently of alterations in blood pressure, dietary intake of sodium and potassium promotes functional changes in the vasculature and lymphatic system. These changes may protect against development of salt-sensitive hypertension. While salt sensitivity cannot be ascribed exclusively to these factors, perturbation of these processes promotes hypertension during high-salt intake. These studies add to the list of genetic and environmental factors that are associated with salt sensitivity, but in particular provide insight into adaptive mechanisms during high salt intake.