Gut microbiota and renin-angiotensin system: a complex interplay at local and systemic levels

Abstract

Gut microbiota is a potent biological modulator of many physiological and pathological states. The renin-angiotensin system (RAS), including the local gastrointestinal RAS (GI RAS), emerges as a potential mediator of microbiota-related effects. The RAS is involved in cardiovascular system homeostasis, water-electrolyte balance, intestinal absorption, glycemic control, inflammation, carcinogenesis and aging-related processes. Ample evidence suggests a bidirectional interaction between the microbiome and RAS. On the one hand, gut bacteria and their metabolites may modulate GI and systemic RAS. On the other hand, changes in the intestinal habitat caused by alterations in RAS may shape microbiota metabolic activity and composition. Notably, the pharmacodynamic effects of the RAS-targeted therapies may be in part mediated by the intestinal RAS and changes in the microbiome. This review summarizes studies on gut microbiota and RAS physiology. Expanding the research on this topic may lay a foundation for new therapeutic paradigms in gastrointestinal diseases and multiple systemic disorders.

The Impact of Gut Microbiome on Maternal Fructose Intake-Induced Developmental Programming of Adult Disease

“…In the high-fructose diet plus 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exposure model, 3,3-dimethyl-1-butanol (DMB) therapy protected against hypertension coinciding with decreased AT1R and increased AT2R protein abundance [ 11 ]. Emerging evidence suggests a bidirectional interaction between the gut microbiome and RAS; gut microbiota-derived metabolites can modulate the gut RAS, while alterations in RAS shape microbiota composition and metabolic activity [ 64 ]. Considering maternal fructose consumption altered gut microbiota and the RAS concurrently, more work is required to explore the interaction between gut microbiome and the RAS implicating the pathogenesis of fructose-induced developmental programming.…”

“…The SCFAs have been used as postbiotics as they are fermentation products of polysaccharides by gut microbiota [ 64 ]. So far, there is only one report showing that maternal high-fructose diet-induced hypertension can be protected by acetate supplementation [ 41 ].…”

Gastroprotective Effect of Azilsartan Through Ameliorating Oxidative Stress, Inflammation, and Restoring Hydroxyproline, and Gastrin Levels in Ethanol-Induced Gastric Ulcer

“… 15 The presence of RAS and their local activity in the GIT have received pronounce attention lately; where many studies showed the involvement of local RAS in the gut in glycemic control and electrolyte regulation, besides having roles in carcinogenesis and inflammatory reactions. 16 Studies showed that blocking angiotensin II receptor AT1 protect against gastric ulcer, 17 , 18 since angiotensin II can generate reactive oxygen species with inducing inflammatory reaction and cellular damage. These effects are mainly mediated through mucosal vasoconstriction.…”

Enalapril Diminishes the Diabetes-Induced Changes in Intestinal Morphology, Intestinal RAS and Blood SCFA Concentration in Rats

“…The intestine is an essential homeostatic organ responsible for nutrient absorption and interaction with abundant gut microbiomes. Some key intestinal processes are regulated by the intestinal RAS, which plays a role in digestion, peptide transport, and water–electrolyte homeostasis [ 14 ]. The intestinal RAS is also a major regulator of glucose uptake in the intestines [ 15 ].…”