The prevalence of maternal obesity has more than doubled in the past two decades with approximately 1 in 5 UK pregnant women now obese [1]. Maternal obesity and excessive gestational weight gain (GWG) constitute some of the most common obstetric risk factors and have direct implications for pregnancy outcome [2]. However, recent evidence suggests that maternal obesity may also have deleterious consequences for the cardiovascular health of the next generation. Mother-child cohort studies have established that both pre-pregnancy BMI and GWG are independently associated with cardio-metabolic risk factors in young adult offspring, including systolic and diastolic blood pressure [3, 4]. Animal models in sheep and non-human primates provide further evidence for the influence of maternal obesity on offspring cardiovascular function, whilst our recent studies in rodents have shown that fetal exposure to the metabolic milieu of maternal obesity may permanently change the regulatory pathways in the hypothalamus that contribute to cardiovascular homeostasis. Leptin plays an important role in the central control of appetite, and is also involved in activation of efferent sympathetic pathways to both thermogenic and non-thermogenic tissues, such as the kidney, and is therefore implicated in obesity-related hypertension. Leptin is also thought to have a neurotrophic role in the development of the hypothalamus and we have recently reported that altered neonatal leptin profiles secondary to maternal obesity were associated with evidence of permanently altered hypothalamic structure and function. Hyperphagia and increased adiposity in the adult offspring of obese rodents is associated with region specific hypothalamic leptin resistance in the appetite regulatory pathways of the arcuate nucleus[5]. We have recently reported compelling evidence from our rodent model that maternal obesity confers persistent sympathoexcitatory hyper-responsiveness and hypertension acquired in the early stages of development. Juvenile offspring develop hypertension as early as 30 days of age and, importantly, prior to the onset of obesity. Hypertension in the offspring of obese rats results from persistent sympathoexcitatory hyper-responsiveness[6] with enhanced cardiovascular stress reactivity, an increase in low/high frequency ratio of heart rate variability (HRV), and increased pressor response to exogenous leptin, all evidence of increased sympathetic tone. Disturbed sympathetic control of blood pressure has not previously been reported as a consequence of maternal obesity. The baroreflex response was also abnormal in OffOb rats (90days) and may also represent a primary programmed defect secondary to maternal obesity. To investigate the role of neonatal hyperleptinaemia in offspring cardiovascular dysfunction, we have treated naive rats with exogenous leptin on postnatal days 9-14. At 1 month of age leptin-treated rats displayed increased mean arterial pressure (MAP) compared to saline treated controls which continued into adulthood. These data provide proof of principle that hyperleptinaemia during a critical window of hypothalamic development may directly lead to adulthood hypertension. These data add to increasing evidence for developmental plasticity in the central efferent pathways of the autonomic nervous system, and further implicates a central role for an acquired selective leptin resistance and ‘hardwiring’ of the developing hypothalamus for a hyperphagic and hypertensive offspring phenotype in offspring of obese rodents. Insight from these animal models raises the possibility that early life exposure to leptin in humans leads to early onset essential hypertension. On-going mother-child cohort and intervention studies in obese pregnant women provide a unique opportunity to address associations between maternal obesity and offspring cardiovascular function.