Pregnancy-induced sympathetic overactivity: A precursor of preeclampsia

Background: Preeclampsia has been shown to constitute a state of sympathetic overactivity. However, it remains unclear if the sympathetic activity precedes preeclampsia or represents only a secondary phenomenon. To further investigate this issue, we performed a prospective study in pregnant women considered to be at increased risk for preeclampsia owing to preeclampsia during a preceding pregnancy. Materials and methods: Twenty-two women with a history of preeclampsia were longitudinally studied on three occasions: twice during pregnancy (M1: 22 ± 4, M2: 33 ± 5 weeks) and once postpartum (M3: 26 ± 6 weeks postpartum). We measured muscle sympathetic nerve activity (MSNA), forearm blood flow, and blood pressure at rest and during reactive hyperaemia after forearm occlusion. Results: At M1 and M2, none of the subjects was hypertensive, however, muscle sympathetic nerve activity levels were significantly augmented, compared with their postpartum values (M1: 21 ± 9, M2: 29 ± 14, M3: 9 ± 5 bursts min^-1; P < 0.05). Forearm vascular resistance did not significantly change from M1 through M3 (M1: 16 ± 9, M2: 15 ± 7, M3: 16 ± 7 U; P = NS). Gestational muscle sympathetic nerve activity values did not differ significantly among the subjects with subsequent preeclampsia compared with those who remained normotensive [with preeclampsia (n = 6): M1: 21 ± 5, M2: 27 ± 6, M3: 7 ± 4 bursts min^-1; without preeclampsia (n = 16): M1: 21 ± 11, M2: 30 ± 16, M3: 9± 6 bursts min^-1; P = NS]. Conclusion: Invariably, all women at risk for preeclampisa showed a pregnancy-induced increase in MSNA (pregnancy-induced sympathetic overactivity, PISO), which normalized after delivery. Most importantly, PISO is not necessarily associated with peripheral vasoconstriction and hypertension. Furthermore, only a subset of patients developed preeclampsia later on. Therefore, we hypothesize that PISO constitutes a precursor of preeclampsia which is physiologically compensated for by vasodilating mechanisms, leading to preeclampsia only when they fail.