Sodium, hypertension, and the gut: does the gut microbiota go salty?

Abstract

Recent evidence suggests that the gut microbiota contributes to the pathogenesis of hypertension (HTN). The gut microbiota is a highly dynamic organ mediating numerous physiological functions, which can be influenced by external factors such as diet. In particular, a major modifiable risk factor for HTN is dietary sodium intake. Sodium consumption in the United States is significantly greater than that recommended by the federal government and organizations such as the American Heart Association. Because of the emerging connection between the gut microbiota and HTN, the interaction between dietary sodium and gut microbiota has sparked interest. High-sodium diets promote local and systemic tissue inflammation and impair intestinal anatomy compared with low sodium intake in both human and animal studies. It is biologically plausible that the gut microbiota mediates the inflammatory response, as it is in constant interaction with the immune system and is necessary for proper maturation of immune cells. Recent rodent data demonstrate that dietary sodium disrupts gut microbial homeostasis as gut microbiota composition shifts with dietary sodium manipulation. In this review, we will focus on gut microbiota activity in HTN and the influence of high dietary sodium intake with an emphasis on the immune system, bacterial metabolites, and the circadian clock.