Intestinal Flora Modulates Blood Pressure by Regulating the Synthesis of Intestinal-Derived Corticosterone in High Salt-Induced Hypertension

Feb 21, 2020Circulation research

Gut Bacteria Influence Blood Pressure by Controlling Intestinal Corticosterone in High Salt Hypertension

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Abstract

A high-salt diet significantly increased blood pressure in Wistar rats.

Fecal microbiota from healthy rats lowered blood pressure in hypertensive rats, while fecal microbiota from high-salt diet-induced hypertensive rats had the opposite effect.
The composition and metabolism of intestinal flora in hypertensive rats were notably altered, with increased corticosterone levels and decreased arachidonic acid levels.
Increased serum corticosterone levels were observed in rats with hypertension, correlating with elevated blood pressure.
Intestinal flora may inhibit high-salt diet-induced production of intestinal-derived corticosterone through its metabolite arachidonic acid.
Fecal microbiota transplantation indicated that intestinal flora play a crucial role in the development of high-salt-induced hypertension.

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RATIONALE: High-salt diet is one of the most important risk factors for hypertension. Intestinal flora has been reported to be associated with high salt-induced hypertension (hSIH). However, the detailed roles of intestinal flora in hSIH pathogenesis have not yet been fully elucidated.

OBJECTIVE: To reveal the roles and mechanisms of intestinal flora in hSIH development.

METHODS AND RESULTS: The abovementioned issues were investigated using various techniques including 16S rRNA gene sequencing, untargeted metabolomics, selective bacterial culture, and fecal microbiota transplantation. We found that high-salt diet induced hypertension in Wistar rats. The fecal microbiota of healthy rats could dramatically lower blood pressure (BP) of hypertensive rats, whereas the fecal microbiota of hSIH rats had opposite effects. The composition, metabolism, and interrelationship of intestinal flora in hSIH rats were considerably reshaped, including the increased corticosterone level and reducedand arachidonic acid levels, which tightly correlated with BP. The serum corticosterone level was also significantly increased in rats with hSIH. Furthermore, the above abnormalities were confirmed in patients with hypertension. The intestinalcould inhibit the production of intestinal-derived corticosterone induced by high-salt diet through its metabolite arachidonic acid. Bacteroides Bacteroides fragilis

CONCLUSIONS: hSIH could be transferred by fecal microbiota transplantation, indicating the pivotal roles of intestinal flora in hSIH development. High-salt diet reduced the levels ofand arachidonic acid in the intestine, which increased intestinal-derived corticosterone production and corticosterone levels in serum and intestine, thereby promoting BP elevation. This study revealed a novel mechanism different from inflammation/immunity by which intestinal flora regulated BP, namely intestinal flora could modulate BP by affecting steroid hormone levels. These findings enriched the understanding of the function of intestinal flora and its effects on hypertension. B fragilis

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Intestinal Flora Modulates Blood Pressure by Regulating the Synthesis of Intestinal-Derived Corticosterone in High Salt-Induced Hypertension

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