Paediatric hypertension is on the rise accompanied by concomitant increase of childhood obesity. The origin of paediatric hypertension however remains unknown. New epidemiological evidence suggests that environmental insult in utero or postnatally may lead to hypertension later in life. Independent associations have been reported between maternal obesity and cardiometabolic disorders in the offspring. In the first part, I will focus on functionally mechanistic pathways of essential hypertension with an attempt to elucidate the rather complex interplay of autonomic dysfunction, leptin, melanocortin-4 receptor (MC4R), inflammation, genetic and epigenetic predispositions. In the second part, the standalone risk factors will be integrated in a flow chart in attempt to understand the deeper meaning of this regulatory machinery in paediatric hypertension. I will refer to the pathophysiology of early sympathetic-mediated hypertension arising from maternal obesity. Maternal diet-induced obesity in rodents permanently resets the responsiveness to leptin-induced SNS in rat offspring via the hypothalamic paraventricular nucleus (PVN)-MC4R pathway. The stimulus that mediates Leptin-SNS-MC4R activity and promotes hypertension is still unknown and remains as a key for future investigations. Future research needs to identify effective preventive measures in the pregnant mother and child to reduce the risk of paediatric hypertension and prevent future cardiovascular disease.
Part of the book: Update on Essential Hypertension