The association between sodium salt and blood pressure is well known. Low salt diets are often recommended for individuals who have high blood pressure, because it is believed that sodium in excess is able to raise blood pressure. While this may be true in certain individuals, the results from studies that have investigated salt restriction as a means to lower blood pressure have been inconclusive. In addition, because high salt diets generally contain other foods that may be considered to be unhealthy, it is difficult to attribute salt directly as a cause of high blood pressure or cardiovascular disease. However, it is known that changes in the levels of ions in extracellular fluid cause changes in the endothelial function, and this might then result in changes to vascular blood flow. Sodium is thought to alter vascular function via an inhibitory effect on nitric oxide (NO), which is also known as endothelium-derived relaxing factor.
Researchers1 have investigated the effects of low salt diets compared with normal salt diets on brachial artery flow-mediated dilatation (FMD). The study involved normotensive overweight and obese subjects in a random cross-over design. Subjects followed a low salt diet (50 mmol N/d) for 2 weeks and then a normal salt diet (150 mmol Na/d) for a further 2 weeks. Both diets were standardised for saturated fat and potassium levels and contained enough calories to ensure maintenance of body weight. The low salt diet resulted in increased dilatation of the brachial artery when compared to the normal salt diet. Those subjects on the low salt diet had lower systolic blood pressure (112 mm Hg) compared to those subjects on the normal salt diet (117 mm Hg). However, the amount of dilatation to the brachial artery was not associated with sodium excretion or with changes in blood pressure.
Reductions in sodium intake clearly cause changes in the endothelium of the brachial artery that results in dilatation. It is known that endothelial dysfunction is one of the clinical symptoms that proceeds cardiovascular disease, and could be involved in its pathogenesis. Because endothelial dysfunction is assessed by flow-mediated dilatation (FMD), the results of this study suggest that high intakes of sodium could be associated with an increased risk of cardiovascular disease, irrespective of blood pressure changes. Nitric oxide is needed for the relaxation of blood vessels, and animal studies suggest that vascular relaxation is impaired with high salt intakes, due to decreases in endothelial NO synthase activity. Human studies have also shown that NO production might be impaired during high sodium diets. It could therefore be the case that sodium reduction benefits vascular function beyond the effects of reduced blood pressure.
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