Estrogen and Bisphenol A in Hypertension
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Abstract
Purpose of Review: Cardiovascular disease (CVD) is a non-subsiding disease that remains a leading cause of morbidity and mortality. CVD has been associated with endocrine disruptors, such as bisphenol A (BPA). This review critically summarizes existing findings on BPA and hypertension, with particular attention to genomic, non-genomic, molecular, and cellular mechanisms of action that render BPA as a cardiovascular estrogenic disruptor. Recent Findings: Owing to its similar estrogenic structure, BPA has been shown to affect various phenotypes that are regulated by the natural hormone, estrogen. Indeed, BPA has been shown to interact with estrogen receptors, located both in the cell membrane and in the cytoplasm/nucleus. Given that estrogen plays an important role in cardiovascular physiology, a contributing role for BPA in CVD would not be unexpected. Existing literature, though limited, established BPA as a source of disruption in cardiovascular health, particularly hypertension. However, effects of BPA are largely dependent on the dose, patient gender, tissue, and developmental stage of the exposed tissue/organ. Summary: Accumulating evidence argues for an adverse effect of BPA on blood pressure, with this effect being gender, dose, and time specific. Thus, comprehensive studies which take these factors and other parameters, like epigenetic factors, into account are warranted before a thorough understanding is at hand. © 2020, Springer Science+Business Media, LLC, part of Springer Nature.
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Bisphenol a, Cardiovascular disease, Environmental pollution, Estrogen, Hypertension, Toxicology, Benzhydryl compounds, Estrogens, Humans, Phenols, 4,4' isopropylidenediphenol, Atrial natriuretic factor, Cyclic amp dependent protein kinase, Endothelial nitric oxide synthase, Estradiol, Estrogen receptor alpha, Estrogen receptor beta, Estrone sulfate, G protein coupled receptor, Mitogen activated protein kinase, Reduced nicotinamide adenine dinucleotide phosphate oxidase, Testosterone, Vasodilator stimulated phosphoprotein, Benzhydryl derivative, Phenol derivative, Blood pressure regulation, Blood vessel tone, Cell membrane, Cell nucleus, Cytoplasm, Diastolic blood pressure, Down regulation, Drug mechanism, Drug receptor binding, Enzyme activation, Enzyme inhibition, Enzyme synthesis, Human, Nonhuman, Pathogenesis, Phenotype, Prenatal exposure, Protein expression, Protein phosphorylation, Review, Signal transduction, Systolic blood pressure, Upregulation, Vasodilatation, Physiology