THE ROLE OF GUT MICROBIOTA IN THE PATHOGENESIS OF HYPERTENSION - NEW PATHOPHYSIOLOGICAL AND THERAPEUTIC PERSPECTIVES

Abstract

Background: Hypertension (HT) is a major cardiovascular risk factor, yet traditional models often fail to explain resistant cases. Recent research shifts the focus to the gastrointestinal tract, positioning gut microbiota as a critical modulator of vascular, renal, and neurological functions. Objective: This study analyzes the role of gut dysbiosis in HT pathogenesis, focusing on gut-vascular and gut-brain axes. It synthesizes evidence on how bacterial metabolites, epigenetic mechanisms, and chronic inflammation affect blood pressure homeostasis, evaluating diet and probiotics as supportive therapies. Methods: A review of the current literature in PubMed, Scopus, Google Scholar and ESH/ESC guidelines was conducted, analyzing metagenomic data, animal model studies, and clinical trials regarding the impact of molecular mechanism of metabolic signaling, epigenetic and immunological processes influencing vascular and renal blood pressure regulation. Results: HT patients exhibit a distinct microbiota phenotype, characterized by an increased Firmicutes/Bacteroides ratio and reduced butyrate-producing bacteria. Key metabolic regulators include protective short-chain fatty acids and prohypertensive trimethylamine N-oxide. It has been demonstrated that leaky gut syndrome leads to the translocation of lipopolysaccharide, which induces systemic neuroinflammation. Furthermore, bacterial metabolites act as epigenetic regulators in the kidneys by modulating the activity of histone deacetylases. Conclusion: Gut dysbiosis is an active pathophysiological component of HT. The gut-vascular axis integrates pressure control through immunological hormonal, and neuronal mechanisms. Incorporating targeted diets, probiotics, and psychobiotics into standard protocols offers promising new perspective for HT management.