Preeclampsia is characterized by a marked increase in peripheral vascular resistance leading to an increase in blood pressure, but the triggering mechanisms are unclear. To determine whether augmented sympathetic vasoconstrictor activity may be an important mechanism in mediating the increase in vasomotor tone, we measured postganglionic sympathetic-nerve activity in the blood vessels of skeletal muscle by means of intraneural microelectrodes in nine women with preeclampsia, eight normotensive pregnant women, six normotensive nonpregnant women, and seven nonpregnant women with hypertension, both at rest and during noninvasive cardiovascular-reflex testing (with the Valsalva maneuver and the cold pressor test). The mean (+/-SE) rate of sympathetic-nerve activity in the normotensive pregnant women (10+/-1 bursts per minute) was not significantly different from that in normotensive nonpregnant women (12+/-2 bursts per minute) or hypertensive nonpregnant women (15+/-3 bursts per minute). In contrast, the rate of sympathetic-nerve activity in the patients with preeclampsia (33+/-3 bursts per minute) was more than three times as high as that in the normotensive pregnant women (P<0.05) and more than twice as high as in the group of nonpregnant women with hypertension (P<0.05). Hemodynamic and sympathetic-nerve responses to both reflex tests did not differ significantly among the four groups. Six patients with preeclampsia were studied again after delivery; mean sympathetic-nerve activity at that time had decreased significantly from the value during pregnancy (from 36+/-4 to 13+/-2 bursts per minute, P<0.01), as had mean arterial pressure (from 118+/-3 to 96+/-1 mm Hg, P<0.01). Preeclampsia is a state of sympathetic overactivity, which reverts to normal after delivery. Our data indicate that the increases in peripheral vascular resistance and blood pressure that characterize this disorder are mediated, at least in part, by a substantial increase in sympathetic vasoconstrictor activity.