Journal
FASEB JOURNAL
Volume 34, Issue 10, Pages 13626-13640Publisher
WILEY
DOI: 10.1096/fj.202001532R
Keywords
DOCA-salt hypertension; endothelial dysfunction; gut microbiota; immune system; probiotics
Categories
Funding
- Ministerio de Economia, Industria y Competitividad, Gobierno de Espana (Ministeri d'Economia, Industria i Competitivitat) [SAF2017-84894-R]
- HHS \ NIH \ National Heart, Lung, and Blood Institute (NHLBI) [HL102033]
- Consejeria de Economia, Innovacion, Ciencia y Empleo, Junta de Andalucia (Ministry of Economy, Innovation, Science and Employment, Government of Andalucia) [CTS164]
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Many probiotics that affect gut microbial ecology have been shown to produce beneficial effects on renin-angiotensin-dependent rodent models and human hypertension. We hypothesized thatBifidobacterium breveCECT7263 (BFM) would attenuate hypertension in deoxycorticosterone acetate (DOCA)-salt rats, a renin-independent model of hypertension. Rats were randomly divided into five groups: control, DOCA-salt, treated DOCA-salt-BFM, treated DOCA-salt-butyrate, and treated DOCA-salt-acetate, for 5 weeks. BFM prevented the increase in systolic blood pressure, cardiac weight, and renal damage induced by DOCA-salt. BFM increased acetate-producing bacterial population and gut acetate levels, improved colonic integrity, normalized endotoxemia, plasma trimethylamine (TMA) levels, and restored the Th17 and Treg content in mesenteric lymph nodes and aorta. Furthermore, BFM improved nitric oxide-dependent vasorelaxation induced by acetylcholine in aortic rings and reduced NADPH oxidase activity in DOCA-salt animals. These protective effects were mimicked by acetate, but not by butyrate supplementation. These data demonstrate that BFM induces changes in gut microbiota linked with attenuation of endothelial dysfunction and increase in blood pressure in this low-renin form of hypertension. These beneficial effects seem to be mediated by increased acetate and reduced TMA production by gut microbiota, thus, improving gut integrity and restoring Th17/Tregs polarization and endotoxemia.
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