The growing epidemic of obesity has attracting increasing interest in the effect of obesity in pregnancy on the developing child. Independent associations have been reported in mother-child cohort studies between maternal obesity and hypertension in the offspring. The mechanisms of early onset hypertension are however less clear. This review focuses on novel advances in our comprehension of sympathetic mediated hypertension. My college and I have previously shown that maternal obesity in rodents leads to sympathetically mediated hypertension in juvenile offspring prior to obesity. This was associated with an exaggerated leptin surge in early postnatal life. Increased leptin during critical periods of development is likely to contribute to the onset of hypertension by altered leptin sensitivity and dysregulation of the neurotropic action of leptin. Unpublished evidence also suggests that the central melanocortin system, including melanocortin 4 receptors, plays a key role in early origins of renal nerve activation and hypertension in offspring of obese rat dams. Renal nerve denervation in juvenile rats restores blood pressure and renal function in neonatal hyperleptineamic rats. The origin of increase renal sympathetic overactivity is unknown but may include central action of renin angiotensin system and melanocortin system in brains regions involved in cardiovascular regulation. Other suggests that peripheral effects including renal ischemia can lead to sympathetic overactivation via central feedforward system. At a time when maternal obesity is reaching epidemic proportions, it appears crucial to better understand the adverse biological processes that mediate the origin of metabolic and cardiovascular dysfunction in the offspring. Recent studies indicate that maternal obesity can permanently influence the leptin-melanocortin system signalling in the offspring and therefore could represent a key mechanism for effecting long-term effects on appetite, renal sympathetic nerve activity and blood pressure.