This narrative review explores how gut dysbiosis influences hypertension, highlighting microbial metabolites' clinical implications.
The gut bacterial microbiome (GBM) plays an emerging role in the pathophysiology of chronic diseases, including hypertension (HTN). Growing evidence suggests that gut dysbiosis, defined by an altered microbial composition and diversity, is involved in the onset and progression of HTN. Exploring the underlying mechanisms linking the GBM and HTN paves the way for novel targeted therapeutic strategies. This narrative review aims to synthesize current data on the interactions between the GBM and HTN, highlight the bidirectional nature of this relationship, and discuss the clinical implications of microbiome modulation in hypertension management. Gut dysbiosis leads to increased intestinal permeability, facilitating systemic translocation of lipopolysaccharides, which in turn activate inflammatory (TLR4, NF-κB) and sympathetic pathways, contributing to endothelial dysfunction and elevated blood pressure. Moreover, certain microbial metabolites, such as short-chain fatty acids (SCFAs), exhibit antihypertensive effects, whereas trimethylamine-N-oxide (TMAO) is associated with increased vascular stiffness and activation of the renin–angiotensin–aldosterone system. The relationship between the GBM and HTN is reciprocal: while dysbiosis can promote HTN, HTN itself may disrupt the gut microbial ecosystem. This bidirectional interaction suggests the existence of a pathological vicious cycle. Innovative strategies to modulate the GBM, including the use of probiotics, prebiotics, postbiotics, and specific dietary interventions such as the Dietary Approaches to Stop Hypertension diet, are currently under investigation. The emergence of pharmacological approaches targeting pathogenic microbial metabolites, such as TMAO, also represents a promising avenue toward precision medicine in hypertension.
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Kakoma et al. (2025) studied this question.
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