A number of recent studies have suggested that when gut bacteria are killed off with antibiotics, patients with hypertension see a drop in blood pressure. Meanwhile, other research has shown that when gut bacteria were transplanted from hypertensive people into normal mice, they developed high blood pressure.
According to the team, the evidence is compelling, but until now, scientists have not identified a mechanism to explain how bacteria increase blood pressure.
The new review, published in the journal Steroids, investigated the linked between the human microbiome and modulators known as glycerrhetinic acid-like factors (GALFs) which are known to disrupt a processes that regulate sodium transport out of human kidney cells – and are believed to play an important role in the development of high blood pressure (hypertension).
"There are probably multiple mechanisms through which gut bacteria can affect hypertension, but this is one that needs to be pursued," said Dr Jason Ridlon, an assistant professor in the the University of Illinois.
Ridlon and his colleagues first discovered the gene for an enzyme in certain bacteria that changes cortisol, a steroid hormone, into another steroid known as an androgen.
He then worked with endocrinologist David Morris at Brown to find that when bacteria break that androgen down further GALFs are produced – and that these disrupt processes that regulate sodium transport, leading to blood pressure rises.
Separate research efforts have also shown that not all gut bacteria metabolise cortisol in the same way, or generate GALFs.
"Two people might have same amount of the bacterium Clostridium scindens, for example, but one person might have the type that has the pathway for generating these steroids. You can only tell by quantifying the genes, but we have to find them first," said Ridlon.
Another recent article, published in the Journal of Lipid Research, does just that, reporting the genes involved in GALF formation in Butyricicoccus desmolans.
"The next step is trying to see if these pathways correlate in patients that have certain forms of hypertension," he commented. "Are there higher abundances of these genes?"
Ridlon said that by being better able to understand what the bacteria are doing, it might be possible to develop new targets and therapies to block the enzymes that produce GALFs in these bacteria.
"It would be great if we could find a targeted solution instead of wiping out everything with antibiotics," he said.
Volume 125, September 2017, Pages 1-13, doi: 10.1016/j.steroids.2017.06.002
“Glucocorticoids and gut bacteria: “The GALF Hypothesis” in the metagenomic era”
Authors: David J.Morris, et al