Sodium, the Vascular Endothelium, and Hypertension: A Narrative Review of Literature.

Abstract

The vascular endothelium and its endothelial glycocalyx contribute to the protection of the endothelial cells from exposure to high levels of sodium and help these structures maintain normal function by regulating vascular permeability due to its buffering effect. The endothelial glycocalyx has negative surface charges that bind sodium and limit sodium entry into cells and the interstitial space. High sodium levels can disrupt this barrier and allow the movement of sodium into cells and extravascular fluid. This can generate reactive oxygen species that inhibit nitric oxide production. This leads to vasospasm and increases intravascular pressures. Overtime vascular remodeling occurs, and this changes the anatomy of blood vessels, their intrinsic stiffness, and their response to vasodilators and results in hypertension. Patients with increased salt sensitivity are potentially at more risk for this sequence of events. Studies on the degradation of the glycocalyx provide insight into the pathogenesis of clinical disorders with vascular involvement, but there is limited information available in the context of higher concentrations of sodium. Data on higher intake of sodium and the imbalance between nitric oxide and reactive oxygen species have been obtained in experimental studies and provide insights into possible outcomes in humans. The current western diet with sodium intake above recommended levels has led to the assessment of sodium sensitivity, which has been used in different populations and could become a practical tool to evaluate patients. This would potentially allow more focused recommendations regarding salt intake. This review will consider the structure of the vascular endothelium, its components, the effect of sodium on it, and the use of the salt blood test mini.