Gut Microbiota as a Mediator of Dietary Salt Effects on Blood Pressure

Dietary sodium excess is a primary driver of hypertension, yet individuals differ markedly in their blood pressure response to salt. This variation, termed salt sensitivity, cannot currently be predicted from clinical variables alone. This review examines three aspects of salt-gut physiology: intestinal sodium handling, salt-induced changes in gut microbiome composition, and microbiota-mediated effects on immune function, metabolite production, and gut barrier integrity. The intestine absorbs dietary sodium through regulated transporters whose activity adapts to luminal and hormonal conditions, making the gut a key regulator of sodium balance. High salt intake consistently alters gut microbiota composition in animal models, most reproducibly depleting <i>Lactobacillus</i> species, with variable effects on overall diversity. These compositional shifts, supported by human data, activate intestinal Th17 cells and deplete short-chain fatty acid producers, contributing to systemic inflammation and elevated blood pressure. The presence of inducible osmoadaptation responses varies substantially across microbes, though activation under dietary sodium conditions has not been demonstrated <i>in vivo</i>. If salt-driven microbial changes contribute causally to hypertension, microbiota-targeted interventions could complement sodium restriction in patients for whom long-term dietary adherence is poor. Controlled sodium intervention studies in animals and humans are needed to establish whether such a causal contribution exists.