Salt-sensitivity of blood pressure (SSBP) affects 50% of the hypertensive and 25% of the normotensive populations. Importantly, SSBP is associated with increased risk for mortality in both populations independent of blood pressure. Despite its deleterious effects, the pathogenesis of SSBP is not fully understood. Emerging evidence suggests a novel role of bile acids in salt-sensitive hypertension and that they may play a crucial role in regulating inflammation and fluid volume homeostasis. Mechanistic evidence implicates alterations in the gut microbiome, the epithelial sodium channel (ENaC), the farnesoid X receptor, and the G protein-coupled bile acid receptor TGR5 in bile acid-mediated effects on cardiovascular function. The mechanistic interplay between excess dietary sodium-induced alterations in the gut microbiome and immune cell activation, bile acid signaling, and whether such interplay may contribute to the etiology of SSBP is still yet to be defined. The main goal of this review is to discuss the potential role of bile acids in the pathogenesis of cardiovascular disease with a focus on salt-sensitive hypertension.
Keywords: ENaC; bile acids; gut microbiome; salt-sensitive hypertension.