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The gut microbiota and blood pressure in experimental models.

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PubMed ID: 30531472

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Jama HA, Kaye DM, Marques FZ

Curr Opin Nephrol Hypertens. Mar 2019. doi: 10.1097/MNH.0000000000000476

COMMENT: This work reviews the evidence that support the relationship between gut microbiota and the development and maintenance of hypertension in experimental models.

MAIN RESULTS:

The use of gnotobiotic animals has allowed knowing the causal link between hipertensive gut microbes and increased blood pressure (BP).

Compared to conventional mice, gnotobiotic mice are protected from developing angiotensin II (Ang II)-induced hypertension (...). Moreover, gnotobiotic Ang II mice have reduced vascular dysfunction. These findings support that, at least in the Ang II context, the gut microbiota is essential for the development of hypertension. Another study performed faecal transplants from two untreated hypertensive and one normotensive individual into gnotobiotic mice (...). After 10 weeks, gnotobiotic mice had developed a similar gut microbiome compared to their donors. Gnotobiotic mice that received faecal transplants from hypertensive donors had significantly reduced microbial diversity and altered composition compared to mice that were transplanted with faeces from the normotensive donor (...).  Strikingly, gnotobiotic mice that received a faecal transplant from hypertensive donors also developed significantly higher systolic and diastolic BP.

Gut dysbiosis has been observed in both genetic and pharmacological models of hypertension. The gut microbiome present in these models is different from their control strains. 

Dietary modification of the gut microbiota could affect blood pressure. Fibre, especially resistant starches, and the short-chain fatty acids (acetate, propionate and butyrate) produced by their fermentation could contribute to get lower blood pressure. On the contrary, a high salt diet increased proinflammatory Th17 inmune cells, which have been implicated in the development of hypertension, and decreased the levels of Lactobacillus murinus in the gut. 

The gut communicates with key tissues involved in hypertension, including the heart, kidney and brain, and could be involved in sympathetic activation.

 CONCLUSIONS:

Over a short period, there has been an exciting and rapid advance in knowledge regarding the role of gut microbiota in the pathogenesis of hypertension. Experimental models, particularly the use of gnotobiotic mice, have been instrumental to determine the causal link between the gut microbiota and hypertension. Moreover, host dietary intake of fibre or supplementation with gut metabolites produced by the fermentation of fibre can modulate BP in hypertensive models. Although probiotics, such as intake of Lactobacillus spp., and even faecal microbiota transplants might seem like an attractive alternative, it is still not clear whether they would benefit patients. The interaction between diet, gut microbiota and host, however, is emerging as potential therapeutic option to help overcome the global burden of hypertension and cardiovascular disease. 

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Raquel Ruiz-Arroyo