Gut Dysbiosis and Western Diet in the Pathogenesis of Essential Arterial Hypertension: A Narrative Review

Abstract

Metabolic syndrome is a cluster of the most dangerous cardiovascular (CV) risk factors including visceral obesity, insulin resistance, hyperglycemia, alterations in lipid metabolism and arterial hypertension (AH). In particular, AH plays a key role in the complications associated with metabolic syndrome. High salt intake is a well-known risk factor for AH and CV diseases. Vasoconstriction, impaired vasodilation, extracellular volume expansion, inflammation, and an increased sympathetic nervous system (SNS) activity are the mechanisms involved in the pathogenesis of AH, induced by Western diet. Gut dysbiosis in AH is associated with reduction of short chain fatty acid-producing bacteria: acetate, butyrate and propionate, which activate different pathways, causing vasoconstriction, impaired vasodilation, salt and water retention and a consequent high blood pressure. Moreover, increased trimethylamine N-oxide and lipopolysaccharides trigger chronic inflammation, which contributes to endothelial dysfunction and target organs damage. Additionally, a high salt-intake diet impacts negatively on gut microbiota composition. A bidirectional neuronal pathway determines the “brain–gut” axis, which, in turn, influences blood pressure levels. Then, we discuss the possible adjuvant novel treatments related to gut microbiota modulation for AH control.

Impact of Helicobacter pylori-Related Metabolic Syndrome Parameters on Arterial Hypertension

“…Specifically, potential causative agents of hypertension include the following (Table 1): (1) genetic factors [12]; (2) diet (particularly sodium and potassium intake, as well as western diet) [13][14][15]; (3) adiposity [16]; (4) hyperinsulinemia and insulin resistance (IR) [17];…”

“…(5) smoking [18]; (6) endothelial dysfunction linked with MetS [19], with excessive release of vasoconstrictive agents and defective secretion of smooth-muscle relaxing mediators, such as nitric oxide [20]; (7) gut microbiota dysbiosis connected with MetS [15,[21][22][23]; (8) inflammatory mechanisms, including pro-inflammatory cytokines and chemokines overexpression, cell infiltration and oxidative stress-all induced by excessive immune system stimulation-that are strongly upregulated in the hypertensive setting [24,25]; (9) innate and adaptive immune system involvement [25,26]; (10) nonalcoholic fatty liver disease (NAFLD), also closely associated with MetS [27]; (11) MetS-related brain neurodegenerative disorders, through disruption to the blood-brain barrier, triggering neuroinflammation, and exacerbation of amyloid disorders and decreased function of the cerebral blood vessels, including reduced cerebral blood flow, altered brain autoregulation, and compromised neurovascular coupling [28][29][30][31]; (12) MetS-related cancer development [32,33].…”

“…In this study, we aimed to investigate the potential impact of H. pylori-related MetS parameters on arterial hypertension, since the triad of H. pylori infection, MetS, and hypertension currently represents a fundamental worldwide health problem on a pandemic scale with high morbidity and mortality, like COVID-19, thereby requiring awareness and appropriate management on a global scale [56,57]. Excessive release of vasoconstrictive agents and defective secretion of smooth-muscle relaxing mediators [17] Gut microbiota dysbiosis Via production, modification, and degradation of microbial-derived bioactive metabolites [15,[21][22][23] Inflammatory mechanisms…”

Healthy Eating Index 2015 and Major Dietary Patterns in Relation to Incident Hypertension; A Prospective Cohort Study

“…On the other hand, reducing potassium intake, in addition to affecting the sodium pump, inhibits potassium channels in the cell membrane and increases intracellular calcium in which eventually leads to HTN [44,45]. All of these factors contribute to the developing of HTN [41].…”

“…This pattern is associated with increased intake of calorie, sodium, saturated fats, and decreased potassium [38,39]. In fact, high sodium intake is the main cause of increased hypertension, which inhibits the sodium pump and stimulates the sodium-calcium exchanger type 1 (NCX1), resulting in increased intracellular calcium concentration, which causes vasoconstriction [40,41]. Additionally, high sodium intake reduces the synthesis of nitric oxide (NO) and increases the plasma level of the endogenous NO inhibitor, which reduces vasodilation [42,43].…”