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.