Prenatal Exposure To Bisphenols Affects Blood Pressure In Both Male And Female Offspring: Differential Role Of Ang Ii

Cardiovascular diseases (CVD) remain the leading cause of death globally and hypertension is one of the prominent risk factors for CVD. Environmental contaminants are often overlooked when assessing disease etiology, but many studies have shown that it is associated with hypertension development. Bisphenols are widely used to manufacture plastics, and we are regularly exposed to these chemicals. Analogs of Bisphenol A (BPA), such as Bisphenol S (BPS) and Bisphenol F (BPF) are frequently used in BPA-free products. However, these chemicals are vastly understudied, and their effects are largely unknown. In order to determine the cardiovascular effects of prenatal exposures to these chemicals, pregnant Sprague Dawley rats were exposed to saline, 5 µg/kg BW of BPA or BPS, or 1 µg/kg BW of BPF. Adult female and male offspring were implanted with radiotelemeters and Systolic (SBP), Diastolic Blood Pressure (DBP), and Mean Arterial Pressure (MAP) were measured for 24 hours. Offspring were sacrificed following data collection, and plasma estradiol (E2) and angiotensin II (Ang II) levels were measured using radioimmunoassay (RIA). Marked differences in BP were observed between the sexes. SBP was significantly increased in BPA and BPS female offspring but only in BPS male offspring compared to controls. BPA-exposed female offspring had higher MAP. BPS-exposed male offspring had a significant increase in HR. As for hormonal levels, E2 levels were found to be significantly higher in BPS female offspring. Ang II levels were unchanged in females but significantly higher in BPF males. These results indicate that exposure to BPA and its analogs BPS and BPF have profound sex-specific effects on hypertension development. It is likely that different pathways are involved in the development of hypertension in the two sexes.