Previous studies suggest some link between
formaldehyde exposure and harmful cardiovascular effects. But whether exposure to
formaldehyde can cause blood pressure to rise, and if so, what the underlying mechanism is, remains unclear. In this study, C57BL/6 male mice were exposed to 0.1, 0.5, 2.5 mg/m3 of gaseous
formaldehyde for 4 h daily over a three-week period. The systolic blood pressure (SBP), diastolic blood pressure (DBP), mean blood pressure (MBP) and heart rate (HR) of the mice were measured by tail-cuff plethysmography, and any histopathological changes in the target organs of
hypertension were investigated. The results showed that exposure to
formaldehyde did cause a significant increase in blood pressure and heart rate, and resulted in varying degrees of damage to the heart, aortic vessels and kidneys. To explore the underlying mechanism, a specific inhibitor of
angiotensin converting enzyme (ACE) was used to block the ACE/AT1R axis. We observed the levels of ACE and
angiotensin II type 1 receptor (AT1R), as well as the
bradykinin (BK) in cardiac cytoplasm. The data suggest that exposure to
formaldehyde induced an increase in the expression of ACE and AT1R, and decreased the levels of BK. Strikingly, treatment with 5 mg/kg/d
ACE inhibitor can attenuate the increase in blood pressure and the pathological changes caused by
formaldehyde exposure. This result has improved our understanding of whether, and how,
formaldehyde exposure affects the development of
hypertension.