Epigenetic inheritance of hypertension

Blood pressure (BP) is influenced by multifactorial risk factors in a combination of genetics and environments. Evidence supports that the cardiovascular diseases (CVD) is initiated during in utero processes. Maternal nutritional environments may play a role in determining fetal growth, BP and subsequent pathophysiology. Studies proposed ill fitted perinatal environments negatively affect healthy fetal growth and developments. Many CVD risk factors, such as nutrition, smoking, pollution, stress, high BP and abnormal BP variability (BPV), have been associated with the modification of epigenetic influences. To modify factors affecting BP and the CVD, investigations are continued exploring mechanisms and the BP regulation, especially in essential hypertension. Some genetic and epigenetic studies have been carried out in the perinatal regulation and fetal development that affect offspring’s morbidity and mortality in later life. As examples, hypertensive-prone spontaneously hypertensive rat strains showed significantly lowered BPs in normotensive uterine and/or nursing environments, while a perinatal low protein diet affected adult offspring’s kidney functions significantly, not to mention sodium sensitivity in gastrointestinal-renal ion transport in BP regulation. A major effect in epigenetics would include DNA methylation, translational histone and noncoding RNA modifications that epigenetic modifications have major functional changes. Although similar to genetic features of DNA heritability, epigenetic mechanisms may differ with potential reversibility by environmental and nutritional factors, which make them potentially crucial for their role in complex and multifactorial diseases. Mechanisms associated with variability and epigenetics are still largely unknown. However, ambulatory BP monitoring (ABPM) as a tool to monitor BP and BPV to detect subtle changes during the subclinical stage to prevent further progress and ultimately make treatment plans before the clinical symptoms appear. Thus, various increased BP and abnormal BPV modifications should be priority tasks in the CVD prevention during the preclinical stages. Understanding the mechanisms and pathology of epigenome that underlie BPV may assist in the better management of hypertensive problems for a predictable reduction of CVD and chronic kidney disease (CKD). Early detection and early intervention in the preclinical stage can save lives and assets.