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.