Effects of Preeclamptic Plasma on Potassium Currents of Human Umbilical Vein Endothelial Cells

Abstract

Endothelial cell (EC) dysfunction in preeclampsia (PE) may be mediated by humoral factors secreted by placenta, thereby affecting the EC vasoactive compound production. Possible targets of these factors include potassium channels, which are important in EC membrane potential control, calcium influx, and vasoactive compound release. Alterations in potassium channel function may thus contribute to the pathogenesis of PE. The present study compared the effects of 10% plasma from PE, normal pregnant (NP), or nonpregnant women (NS) on potassium currents of human umbilical vein ECs (HUVECs), using whole-cell patch clamp technique, with HUVECs in conventional culture medium (10% fetal bovine serum) as controls. Cells of all groups were similar in morphology and whole-cell capacitance. The fraction of cells with inward rectifier potassium channel (IRK) current in PE plasma (41.2%) was significantly lower than those in NP and NS plasmas (76.9% and 59.1%, respectively), although the IRK current density was similar among groups. The outward current components included the calcium-sensitive potassium channels (K(Ca)) and were partially blocked by 100 nmol/L apamin and 200 nmol/L iberiotoxin. The fraction with outward current in PE plasma (100%) was significantly higher than those in NP and NS plasmas (76.9% and 81.8%). The findings indicate inhibition of IRK expression by PE plasma in HUVEC culture, while K(Ca) expression may be facilitated probably as a compensatory response to diminished IRK. These data suggest that potassium channels may be a target of the pathogenic factor/factors in the plasma of patients with PE and may play roles in the pathogenesis of this condition.