Gut microbiota modulates stress-induced hypertension through the HPA axis

Jun 15, 2020Brain research bulletin

Gut bacteria may influence stress-related high blood pressure through the body's stress response system

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Abstract

Stress-induced hypertension (SIH) is linked to a hyperactive hypothalamus-pituitary-adrenal (HPA) axis and altered gut microbiota.

Rats with SIH exhibited increased levels of adrenocorticotropic hormone (ACTH) and corticosterone (CORT).
The expression of corticotropin-releasing hormone (CRH) was elevated in the paraventricular nucleus of the hypothalamus in SIH rats.
Decreased glucocorticoid receptor (GR) expression and increased corticotropin-releasing factor receptor 1 (CRFR1) were observed in the hypothalamus of SIH rats.
Treatment with antibiotics to delete gut microbiota reduced HPA axis hyperactivity and lowered stress-induced blood pressure increases.
The findings suggest a potential link between gut microbiota alterations and the dysfunction of the HPA axis in the context of SIH.

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Stress is associated with an increased risk of hypertension, and the incidence of stress-related hypertension has risen rapidly in recent years; however, the underlying mechanisms remain elusive. Gut dysbiosis has been demonstrated to contribute to hypertension and hyperactivation of the hypothalamus-pituitary-adrenal (HPA) axis. Based on our previous findings showing the altered gut microbiota in the rats of stress-induced hypertension (SIH), the present study aims to investigate whether the stress-induced alteration in gut microbiota can lead to the dysfunction of the HPA axis which contributes to the development of SIH. SIH was developed in rats subjected to electric foot-shock combined with buzzer noise stressors. The gut microbiota of rats were deleted by administering an antibiotic cocktail containing ampicillin (1 g/L), vancomycin (500 mg/L), neomycin (1 g/L), and metronidazole (1 g/L) in drinking water. The serum levels of adrenocorticotropic hormone (ACTH) and corticosterone (CORT) were tested using enzyme-linked immunosorbent assay (ELISA). The mRNA expression of glucocorticoid receptor (GR) and corticotropin-releasing factor (CRF), CRFR1 and CRFR2 was detected by quantitative reverse transcription polymerase chain reaction (qRT-PCR). The cellular protein expressions of corticotropin-releasing hormone (CRH), c-fos, and GR were examined by immunohistochemical staining. In the present study, SIH rats showed a hyperactive HPA axis as indicated by the increased CRH expression in the paraventricular nucleus (PVN) of the hypothalamus, the elevated serum ACTH or CORT concentrations, and increased adrenal gland index. The decreased GR expression and increased CRFR1 in the hypothalamus might underlie the hyperactivation of the HPA axis. The microbial deletion by antibiotics mitigated the hyperactivation of the HPA axis and attenuated the stress-induced elevation of blood pressure, indicating that the causal link of gut microbiota to SIH is mediated, at least in part, by the HPA axis activity. Our findings shed new light on the mechanisms underlying SIH.

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Gut microbiota modulates stress-induced hypertension through the HPA axis

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