This would be cool because of the side effects of hypertension medications.
Gut Microbiota Potential for a Unifying Hypothesis for Prevention and Treatment of Hypertension
Despite
major advances in pharmacological and device-based therapies, systemic
hypertension (HTN) continues to be the major, modifiable risk factor for
most cardiovascular disease and a leading cause of morbidity and
mortality. Treatment resistant HTN (RH) is present in ≈15% to 20% of
hypertensive patients, with few treatment options. These facts provide
an opportunity to develop novel hypotheses to advance this field.
Over 60 years ago, Irvine Page1
proposed a mosaic theory where interplay of multiple factors integrate
to increase blood pressure (BP). This fostered establishment of
cellular, molecular, and physiological mechanisms altered in HTN.
However, how these diverse factors integrate to impair BP control
remains a challenge. Furthermore, why some factors are prohypertensive
in one individual and not in another, and where prohypertensive signals
originate, remains an enigma.
In this Viewpoint, we
propose that the gut and gut microbiota could be one missing link and
provide a potential unifying concept. We summarize most recent evidence
for involvement of gut microbiota in BP control and HTN. We present our
thoughts on the current state and relevant knowledge gaps to be
addressed to determine whether targeting gut microbiota and related
pathology would be a next frontier in HTN therapeutics.
Are HTN or RH Associated With a Unique Gut Microbial Signature?
Gut
dysbiosis and microbial functions contribute to pathological effects
beyond the gastrointestinal system. Gut microbiota play a role in BP
regulation, and gut dysbiosis has been observed in multiple animal
models of HTN.2–5 Our group was among the first to document HTN-associated gut dysbiosis and an increased Firmicutes/Bacteroidetes ratio.2,3
This was associated with a decrease in acetate- and butyrate-producing
bacteria and an increase in the lactate-producing bacteria. High-fiber
diet and acetate supplementation correct gut dysbiosis, increase the
abundance of acetate-producing bacteria, and are associated with lower
BP in DOCA-salt mice.5
Stroke-prone spontaneously hypertensive rats exhibit gut dysbiosis, and
fecal microbiota transplant (FMT) from stroke-prone spontaneous
hypertensive rats to Wistar–Kyoto normotensive rats increases BP.4
Furthermore, we noted that HTN is associated with profound pathological
changes in the gut and increases brain–gut transmission in animal
models of HTN.6
Microbial dysbiosis has also been observed in patients with high BP.2,3 Interestingly, subjects with HTN or pre-HTN demonstrate similar characteristic changes in gut microbiota composition.7
In a RH patient, antibiotic treatment resulted in BP under control with
only an angiotensin-converting enzyme inhibitor, suggesting possible
involvement of gut microbiota in the pathogenesis of RH as antibiotics
alter gut microbiota.8
Future work will be needed to determine whether a unique microbial
signature in the gut, gut pathology, and increased brain–gut–bone marrow
connection are present in patients with RH.
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