There is increasing evidence of the gut microbiota’s influence on hypertension and its complications, such as myocardial infarction, heart failure, stroke, chronic kidney disease. This is not unexpected when the most common risk factors for hypertension, such as diet, medication, sex, and age, are concerned, impacting the gut microbiota. For example, sodium and fermentable fiber have been studied concerning both hypertension and gut microbiota. The receptors that bind these metabolites have also been explored with positive findings—examples include known short-chain fatty acid receptors, such as G-protein coupled receptors OLF78, GPR109a, GPR43, and GPR41 in mice. OLF78 and GPR41 have been studied to have inverse blood pressure regulation roles, whereas GPR43 and GPR109A have been demonstrated to impact cardiac function. However, the underlying mechanisms remain crudely understood, and translation to hypertensive patients is still required.
In animal models, directly targeting the gut microbiota has been a fruitful approach in the TMA-inhibitor cases, 3,3-dimethyl-1-butanol, albeit not for hypertension. The primary issue faced here is the disparity between interventions in animal versus clinical studies, with the latter lacking. Both BP and the gut microbiota are, independently, highly problematic. Studies are being carried out to understand how different microbial communities affect gut microbiota. It is also essential to accept the limitations of sequencing the microbiome—we are only scratching the surface with the identification of mostly bacteria, to date, while ignoring other critical components in the microbiota.
In conclusion, following recent guidelines to improve the quality of the design, collection, and analysis of microbial datasets will enhance the reproducibility and, hopefully, the translatability of findings, which will be essential to advance the field and move from association to causation to intervention.
Ref: https://www.ahajournals.org/doi/full/10.1161/HYPERTENSIONAHA.120.14473
