The clinical presentation of pre-eclampsia suggests that microvascular dysfunction may play a role in the maternal manifestations of the disease. Isovolumetric venous pressure ( P V i ) is an index of microvascular function, reflecting local plasma colloid osmotic (oncotic) pressure, and is abnormal in clinical conditions with microvascular dysfunction. We hypothesized that, in pre-eclampsia, post-capillary margination of neutrophils would increase post-capillary resistance, and therefore P V i . A small cumulative step strain-gauge plethysmography protocol was used to compare P V i in 18 women with pre-eclampsia, 16 normal pregnant women and 17 non-pregnant controls. Circulating levels of vascular cell-adhesion molecule-1 (VCAM-1), intercellular cell-adhesion molecule-1 (ICAM-1) and E-selectin, and neutrophil elastase, were measured to assess endothelial and neutrophil activation respectively. P V i was significantly greater in the pre-eclampsia group, relative to the normal pregnant and non-pregnant controls ( P <0.001, ANOVA, for both comparisons). P V i was significantly lower during normal pregnancy compared with the non-pregnant controls ( P = 0.001). Plasma levels of neutrophil elastase, VCAM-1, ICAM-1 and E-selectin ( P = 0.001) were significantly greater in the pre-eclamptics than the controls. Significant positive correlations were observed between P V i and neutrophil elastase ( r = 0.71, P = 0.001), VCAM-1 ( r = 0.52, P = 0.03), ICAM-1 ( r = 0.67, P = 0.002), E-selectin ( r = 0.69, P = 0.001), uric acid levels ( r = 0.54, P = 0.02) and haematocrit ( r = 0.64, P = 0.004) in pre-eclampsia. The relationship with the platelet count was negative ( r =-0.65, P = 0.003). No significant correlations were observed between P V i and maternal age, gestational age, total protein, albumin, diastolic blood pressures, age, body mass index and infant birth mass in the normal pregnant and non-pregnant controls. These data suggest that microvascular dysfunction occurs in pre-eclampsia, and that it is related to alterations in endothelial cell and neutrophil activation.