Antihypertensive Effects of Probiotics

Robles-Vera, Iñaki; Toral, Marta; Romero, Miguel; Jiménez, Rosario; Sánchez, Manuel; Pérez‐Vizcaíno, Francisco; Duarte, Juan

doi:10.1007/s11906-017-0723-4

Cited by 106 publications

(59 citation statements)

References 60 publications

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“…Nevertheless, we also found that acetate prevented endothelial dysfunction induced by AngII in a GPR-independent manner, because it was unaffected by its antagonists. A reduced GPR-41 expression in aorta has been associated to reduced plasma butyrate levels and high BP in spontaneously hypertensive rats, as compared to Wistar-Kyoto rats (Robles-Vera et al, 2017;Kim et al, 2018). Interestingly, we found that AngII downregulated both GPR41 and GPR43 in endothelial cells.…”

Section: Discussionmentioning

confidence: 48%

Protective Effects of Short-Chain Fatty Acids on Endothelial Dysfunction Induced by Angiotensin II

et al. 2020

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Short-chain fatty acids (SCFAs) are among the main classes of bacterial metabolic products and are mainly synthesized in the colon through bacterial fermentation. Short-chain fatty acids, such as acetate, butyrate, and propionate, reduce endothelial activation induced by proinflammatory mediators, at least in part, by activation of G protein-coupled receptors (GPRs): GPR41 and GPR43. The objective of the study was to analyze the possible protective effects of SCFAs on endothelial dysfunction induced by angiotensin II (AngII). Rat aortic endothelial cells (RAECs) and rat aortas were incubated with AngII (1 µM) for 6 h in the presence or absence of SCFAs (5-10 mM). In RAECs, we found that AngII reduces the production of nitric oxide (NO) stimulated by calcium ionophore A23187; increases the production of reactive oxygen species (ROS), both from the nicotinamide adenine dinucleotide phosphate oxidase system and the mitochondria; diminishes vasodilator-stimulated phosphoprotein (VASP) phosphorylation at Ser 239 ; reduces GPR41 and GPR43 mRNA level; and reduces the endothelium-dependent relaxant response to acetylcholine in aorta. Coincubation with butyrate and acetate, but not with propionate, increases both NO production and pSer 239 -VASP, reduces the concentration of intracellular ROS, and improves relaxation to acetylcholine. The beneficial effects of butyrate were inhibited by the GPR41 receptor antagonist, β-hydroxybutyrate, and by the GPR43 receptor antagonist, GLPG0794. Butyrate inhibited the down-regulation of GPR41 and GPR43 induced by AngII, being without effect acetate and propionate. Neither β-hydroxybutyrate nor GLPG0794 affects the protective effect of acetate in endothelial dysfunction. In conclusion, acetate and butyrate improve endothelial dysfunction induced by AngII by increasing the bioavailability of NO. The effect of butyrate seems to be related to GPR41/43 activation, whereas acetate effects were independent of GPR41/43.

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Section: Discussionmentioning

confidence: 48%

Protective Effects of Short-Chain Fatty Acids on Endothelial Dysfunction Induced by Angiotensin II

et al. 2020

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“…Regarding antihypertensive drugs, no specific study has investigated the effect of drugs on the gut microbiota. In contrast, many studies have shown that probiotics may have antihypertensive effects [243].…”

Section: Cardiovascular-renal Crosstalk Cardiorenal Syndromes and Tmentioning

confidence: 96%

Gut microbiota and inflammation in chronic kidney disease and their roles in the development of cardiovascular disease

et al. 2018

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The health and proper functioning of the cardiovascular and renal systems largely depend on crosstalk in the gut-kidney-heart/vessel triangle. Recent evidence suggests that the gut microbiota has an integral function in this crosstalk. Mounting evidence indicates that the development of chronic kidney and cardiovascular diseases follows chronic inflammatory processes that are affected by the gut microbiota via various immune, metabolic, endocrine, and neurologic pathways. Additionally, deterioration of the function of the cardiovascular and renal systems has been reported to disrupt the original gut microbiota composition, further contributing to the advancement of chronic cardiovascular and renal diseases. Considering the interaction between the gut microbiota and the renal and cardiovascular systems, we can infer that interventions for the gut microbiota through diet and possibly some medications can prevent/stop the vicious cycle between the gut microbiota and the cardiovascular/renal systems, leading to a decrease in chronic cardiovascular and renal diseases.

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“…Probiotics can be selectively used to introduce and expand new types of microorganisms. Probiotics exert antihypertensive effects in human hypertensive patients and rat with genetic hypertension (genetic hypertensive rats) . In fact, chronic consumption of Lactobacillus strains not only reduced BP, but also inhibited organ target damage and improved endothelial dysfunction in spontaneously hypertensive rats (SHR) .…”

Section: Introductionmentioning

confidence: 99%

The Probiotic Lactobacillus fermentum Prevents Dysbiosis and Vascular Oxidative Stress in Rats with Hypertension Induced by Chronic Nitric Oxide Blockade

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et al. 2018

Molecular Nutrition Food Res

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Antihypertensive Effects of Probiotics

Cited by 106 publications

References 60 publications

Protective Effects of Short-Chain Fatty Acids on Endothelial Dysfunction Induced by Angiotensin II

Protective Effects of Short-Chain Fatty Acids on Endothelial Dysfunction Induced by Angiotensin II

Gut microbiota and inflammation in chronic kidney disease and their roles in the development of cardiovascular disease

The Probiotic Lactobacillus fermentum Prevents Dysbiosis and Vascular Oxidative Stress in Rats with Hypertension Induced by Chronic Nitric Oxide Blockade

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