Salt sensitivity of blood pressure. From renal mechanisms to immune and inflammatory pathways

The variability in blood pressure response to dietary salt intake, salt sensitivity (SS), is an important factor in cardiovascular health. This narrative review aims to provide an update on the mechanisms underlying SS, including impaired renal sodium handling and endothelial dysfunction, and discuss its prognostic implications for hypertension and cardiovascular risk.

The classic Guyton theory attributes SS to impaired renal sodium handling, leading to volume expansion and increased blood pressure. The vascular dysfunction theory emphasizes endothelial dysfunction, where impaired vasodilation elevates blood pressure. Inflammation significantly impacts SS, with pro-inflammatory cytokines exacerbating vascular and renal damage. Gene variants affecting sodium handling and blood pressure regulation interact with environmental factors to shape the SS phenotype. SS predicts future hypertension risk in normotensive men with varying salt sensitivity levels. In a study of sixty-two SS and ninety-four salt-resistant (SR) hypertensive patients, SS emerged as an independent cardiovascular risk factor. A long-term follow-up involving 278 hypertensive and 430 normotensive individuals linked SS to increased mortality risk. However, evidence supporting SS as an independent prognostic factor remains weak, primarily based on two studies with limited participants. Residual confounding complicates results interpretation.

The World Health Organization recommends public health policies of salt intake reduction. Salt intake reduction is safe and cost-effective when implemented as part of a population strategy of primary prevention. Studying genetic, inflammatory, and lifestyle factors implicated in SS remains a clinical research priority for personalizing management strategies aimed at preventing cardiovascular disease.