Hypertension is an important modifiable risk factor for cardiovascular diseases. Its high prevalence, combined with the significant morbidity and mortality associated with secondary complications, make it a major public health concern. Despite decades of research, over 95% of all cases of hypertension remain of unknown etiology, necessitating that treatments target the established symptoms and not the cause. One of the important recent advances in hypertension research is an understanding that hypertension often may have a developmental origin. A substantial body of evidence indicates that exposure to an adverse intrauterine environment during critical periods of development may predispose an individual to develop hypertension later in life. A causative mechanism has yet to be identified, but may include epigenetic modifications, and/or alterations in renal, vascular or autonomic cardiovascular functions. This review will present evidence regarding changes in autonomic activity as a possible causative pathophysiological mechanism underlying the development of programmed hypertension. In man, low birth weight is the best-known risk factor for hypertension of developmental origins, although this is a broad surrogate measure for intrauterine adversity. This review will include clinical studies across the lifespan that have investigated autonomic function in individuals with fetal growth restriction and those born preterm. A determination of whether altered autonomic function is seen in these individuals in early life is imperative, as hypertensive disorders that have their origins in utero, and that can be identified early, will open the door to risk stratification, and the development of new strategies that prevent or specifically target these mechanisms.