To summarize evidence supporting that microorganisms colonizing our gastrointestinal tract, collectively known as the gut microbiota, are implicated in the development and maintenance of hypertension in experimental models.
The use of gnotobiotic (germ-free) mice has been essential for advancement in this area: they develop higher blood pressure (BP) if they receive faecal transplants from hypertensive patients compared to normotensive donors, and germ-free mice have a blunted response to angiotensin II. Experimental hypertension is consistently accompanied by changes in the composition of the gut microbiota. This is combined with a shift in microbial diversity and the deterioration of the gut epithelial barrier commonly referred to as gut dysbiosis. Restoration of normal gut biosis and microbiota alleviates and protects against the development of hypertension in both genetic and pharmacological models. This has been achieved by the use of antibiotics, faecal transplants between normotensive and hypertensive strains, and the use of prebiotics (i.e. food stuff that feeds the microbiota), probiotics (i.e. live bacteria) and gut metabolites (i.e. short-chain fatty acids).
Research into experimental hypertension supports that the gut microbiota contributes to the regulation of BP. Manipulation of the microbiota might represent a new tool to prevent hypertension.
aHeart Failure Research Group, Baker Heart and Diabetes Institute
bDepartment of Pharmacology, Faculty of Medicine Nursing and Health Sciences, Monash University
cCentral Clinical School, Faculty of Medicine Nursing and Health Sciences, Monash University
dHeart Centre, Alfred Hospital
eSchool of Biological Sciences, Faculty of Science, Monash University, Melbourne, Victoria, Australia
Correspondence to Dr Francine Z. Marques, Hypertension Research Laboratory, Monash University, Victoria 3800, Australia. E-mail: firstname.lastname@example.org