Non‐Technical Summary  In young men, sympathetic nerve activity is directly related to the level of vasoconstrictor tone in the peripheral vasculature. However, in young women this relationship does not exist, suggesting that certain factors (potentially related to the female sex hormones) offset the transfer of sympathetic nerve activity into vasoconstrictor tone in this population. In the present study we show that, in young women, the β‐adrenergic receptors (which cause vasodilatation in response to noradrenaline) blunt the vasoconstrictor effect of resting sympathetic nerve activity in young women. This mechanism does not occur in young men or postmenopausal women. It is possible that the β‐adrenergic receptors may partially protect young women against the sometimes harmful effects of high sympathetic nerve activity. This may explain why the risk of developing hypertension is greater in young men and postmenopausal women (who have very high sympathetic nerve activity) compared to young women.   In men, muscle sympathetic nerve activity (MSNA) is positively related to total peripheral resistance (TPR) and inversely related to cardiac output (CO). However, this relationship was not observed in young women. We aimed to investigate whether simultaneous β‐adrenergic stimulation offsets this balance in young women. Furthermore, we aimed to examine whether the ability of the β‐adrenergic receptors to offset the transduction of MSNA into vasoconstrictor tone was lost in postmenopausal women. We measured MSNA (peroneal microneurography), arterial pressure (brachial line), CO (Modelflow), TPR and changes in forearm vascular conductance (FVC) to increasing doses of noradrenaline (NA; 2, 4 and 8 ng (100 ml)−1 min−1) before and after systemic β‐blockade with propranolol in 17 young men, 17 young women and 15 postmenopausal (PM) women. The percentage and absolute change in FVC to the last two doses of NA were greater during β‐blockade in young women (P < 0.05), whereas the change in FVC was similar before and during β‐blockade in young men and PM women (P > 0.05). Before β‐blockade there was no relationship of MSNA to TPR or mean arterial pressure (MAP) in young women. Following β‐blockade, MSNA became positively related to TPR (r= 0.59, P < 0.05) and MAP (r= 0.58, P < 0.05). In the PM women and young men, MSNA was positively associated with TPR. β‐Blockade had no effect on this relationship. Our data suggest that the β‐adrenergic receptors offset α‐adrenergic vasoconstriction in young women but not young men or PM women. These findings may explain in part the tendency for blood pressure to rise after menopause in women.