The Microbiome and Blood Pressure: Can Microbes Regulate Our Blood Pressure?

Abstract

The surfaces of the human body are heavily populated by a highly diverse microbial ecosystem termed the microbiota. The largest and richest among these highly heterogeneous populations of microbes is the gut microbiota. The collection of microbes and their genes, called the microbiome, has been studied intensely through the past few years using novel metagenomics, metatranscriptomics, and metabolomics approaches. This has enhanced our understanding of how the microbiome affects our metabolic, immunologic, neurologic, and endocrine homeostasis. Hypertension is a leading cause of cardiovascular disease worldwide; it contributes to stroke, heart disease, kidney failure, premature death, and disability. Recently, studies in humans and animals have shown that alterations in microbiota and its metabolites are associated with hypertension and atherosclerosis. In this review, we compile the recent findings and hypotheses describing the interplay between the microbiome and blood pressure, and we highlight some prospects by which utilization of microbiome-related techniques may be incorporated to better understand the pathophysiology and treatment of hypertension.

Keywords: blood pressure; dysbiosis; hypertension; lifestyle; microbial metabolites; microbiota; short-chain fatty acid.

Figure 1

Methodologies used to study the human microbiome. The human body harbors large amounts of microbes that vary from one site to another. From each specific site, microbes can be studied in various ways depending on the samples isolated. Those tools range from metagenomics, metatranscriptomics to metaproteomics and metabolomics. Based on the approach and platform used, results include composition of the microbial communities, microbial genes function, gene expression or proteins levels, and metabolites activities.

Figure 2

Proposed hypotheses for microbiota relationship to blood pressure. SCFA, short-chain fatty acids; SNS, sympathetic nervous system; ACE, angiotensin-converting enzyme; FXR, farnesoid X receptor.