Sex differences in the risk of hypertension are well recognized: prior to the menopause, women have a decreased risk of hypertension and other cardiovascular diseases compared to men. Conversely, hypotensive disorders such as orthostatic hypotension are more common in young women. Even among normotensive individuals, women tend to have lower blood pressure, and lower peripheral sympathetic vasoconstrictor nerve activity (SNA) compared to men. These differences disappear (or are reversed) at menopause. Although protective vasodilator effects of estrogen on vascular function have been demonstrated, integrative mechanisms for sex differences in blood pressure control remain poorly understood. In recent years it has become increasingly clear that inter-individual differences in mechanisms controlling blood pressure (sympathetic nerve activity, cardiac output, vascular responsiveness) provide important insight into its regulation. In this context, resting levels of SNA are extremely variable, and can show a range of as much as 7 – 10 fold in a healthy young population. It is an important (although initially puzzling) characteristic of SNA that in general there is no relationship between SNA and arterial pressure among young normotensive humans: people with higher resting SNA do not necessarily have higher blood pressure. This relationship becomes positive in older individuals, and is particularly strong in post-menopausal women; these latter factors likely contribute to the increased risk of hypertension with aging. The mechanisms for the lack of SNA-BP relationship in young people, and changes in these mechanisms as functions of sex and aging have been the focus of our recent investigations. Among normotensive young men, a direct relationship exists between muscle SNA and total peripheral resistance (TPR), suggesting that muscle SNA is a good index of whole body vasoconstrictor tone in this group. An inverse relationship exists between SNA and cardiac output, and men with higher SNA also show blunted vasoconstriction to adrenergic agonists. These latter observations have provided insight into the variable role of SNA in blood pressure control among young healthy men: men with higher SNA have lower cardiac output and less adrenergic responsiveness, thus “balancing” the potential pressor effects of high SNA. Surprisingly, the SNA-TPR and SNA-cardiac output relationships do not exist in young women, suggesting that sympathetically mediated vasoconstriction is modified by other factors associated with female sex and/or sex hormones. Our recent data suggest that beta-adrenergic-mediated vasodilation may offset alpha-adrenergic vasoconstriction in young women, thus contributing to the differences in blood pressure regulation between sexes. In young women, systemic beta-adrenergic blockade augmented forearm vasoconstrictor responses to norepinephrine. Furthermore, the relationship between SNA and TPR (which was absent before beta blockade) became significant and positive with beta blockade. Importantly, these effects of beta adrenergic blockade were not observed in young men or in post-menopausal women, in whom significant, positive SNA-TPR relationships existed both pre- and post-beta blockade. Taken together, these data point to integrated autonomic mechanisms which differ between men and women in control of vascular resistance and blood pressure. The changes seen at menopause suggest that female sex steroids are important modulators of sympathetic neurovascular interactions in women, and that beta-adrenergic vasodilation is an important contributor to this modulation.