The well-documented epidemiologic association of insulin levels and blood pressure have raised the possibility of a role for insulin in the pathogenesis of essential hypertension. The sympathetic nervous system (SNS) is a possible link in this relationship, since insulin is a critical mediator of dietary-induced changes in sympathetic activity. Insulin mediated glucose metabolism, in central neurons related anatomically to the ventromedial hypothalamus, mediates fasting-induced suppression, and overfeeding-induced stimulation of the SNS. The effect of insulin to stimulate the SNS is readily demonstrable in humans. The physiological role of insulin-mediated sympathetic stimulation is in the regulation of dietary thermogenesis, the linkage between dietary intake and metabolic rate. The association of hyperinsulinemia with hypertension in the obese led to the hypothesis that insulin-mediated sympathetic stimulation, recruited in the obese to increase metabolic rate and restore energy balance, had the unintended consequence of increasing blood pressure. Data developed in a population based cohort (The Normative Aging Study, NAS) support this hypothesis since: obesity was associated with evidence of increased SNS activity; there was a demonstrable relationship between glucose and insulin levels and SNS activity; and blood pressure was associated with both insulin and sympathetic activity, a relationship that was noted in the population as a whole after adjustment for body mass index and body fat distribution. Interruption of hyperinsulinemia in obese subjects, furthermore, decreased both plasma NE level and blood pressure. These data provide evidence that insulin-mediated sympathetic stimulation contributes to hypertension in the NAS population, and that the relationship occurs in both obese and non-obese subjects.