DISTURBED NITRIC-OXIDE ENDOTHELIN-1 EQUILIBRIUM IN CULTURED HUMAN PLACENTAL ENDOTHELIOCYTES IN PREECLAMPSIA

Several observations suggest that endothelial cell dysfunction is a ce ntral pathophysiologic event of preeclampsia. Endothelin-l (ET-1) is a vasoconstrictor peptide of the endotheliocyte and is increased in the sera of preeclamptic patients. The aim of this study was to investiga te the possible regulatory mechanisms between ET-1 and nitric oxide (N O) production in cultured placental endotheliocytes. We report that en dothelial cells of arterial placental blood vessels show a dysfunction al mechanism of negative feedback regulation of ET-1 production by cGM P or insufficient NO release in response to a stimulus in the form of an increasing ET-1 concentration.