作者: Ting Deng , Xiaoman Xie , Jiufei Duan , Mingqing Chen
DOI: 10.1016/J.ENVPOL.2019.01.099
关键词:
摘要: Epidemiological studies and animal experiments have suggested that exposure to Di-(2-ethylhexyl) phthalate (DEHP) is strongly associated with an increase in blood pressure. However, the mechanisms result detrimental effects of DEHP on pressure are unclear. In our study, mice were orally exposed dosages 0.1, 1, 10 mg/kg/day for 6 weeks. The results showed could induce a significant systolic (SBP) heart rate, thickening ventricular wall. To explore underlying mechanism, we measured level of: angiotensin converting enzyme (ACE); bradykinin B2 receptor (BK2R); endothelial nitric oxide synthase (eNOS); Ca2+ cardiac cytoplasm as well serum (NO). ACE levels, decrease levels. Moreover, BK2R, Ca2+, eNOS NO decreased when DEHP. Interestingly, 5 mg/kg/day inhibitor (ACEI) treatment inhibited pressure, levels eNOS, NO, induced by exposure. Our suggest might activating expression, inhibiting bradykinin-NO pathway.