4.3.2. SCFAs and Their Receptors

Notably, an association between microbiota-derived metabolites and hypertension has been found in several models of developmental hypertension [43,93,94,106].

SCFAs, the main metabolites produced by the gut microbiota, have one to six carbon atoms (C1–C6), mainly consisting of acetic acid (C2), propionic acid (C3), and butyric acid (C4) [88]. In SHR, hypertension is associated with decreased abundance of acetateand butyrate-producing bacteria [15]. Similarly, SCFAs and their receptors are involved in hypertension of developmental origins, as reported in several animal models [52,93,106].

In a model of maternal administration of minocycline, minocycline-induced hypertension is associated with a reduction of plasma acetate and butyrate [52]. Another report demonstrated that dam rats receiving a 60% fructose diet caused offspring's hypertension, coinciding with an increased plasma acetate level and a reduction of renal GPR41 and GPR43 expression [93]. As acetate is a ligand for GPR41 to induce vasodilatation, and Olfr78 exhibits vasoconstrictive action [109], these findings support the notion that SCFAs and their receptors contribute to maternal high-fructose-diet-induced hypertension in adult offspring. Additionally, maternal garlic oil therapy protects against offspring hypertension programmed by a high-fat diet, which is related to increased acetate, butyrate, and propionate, as well as their producing microorganisms [110]. Moreover, maternal SCFA supplementation have been reported to be protective on hypertension of developmental origins [85,94]. These findings support the notion that SCFAs and their receptors might be a crucial mechanism behind developmental programming of hypertension.
