Disturbed nitric oxide/endothelin-1 equilibrium in cultured human placental endotheliocytes in preeclampsia

B Leszczyńska-Gorzelak, J Oleszczuk, K Kamiński, D Szymula, M Gorzelak, J J Oleszczuk
Gynecologic and Obstetric Investigation 1998, 46 (3): 145-9
Several observations suggest that endothelial cell dysfunction is a central pathophysiologic event of preeclampsia. Endothelin-1 (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 investigate the possible regulatory mechanisms between ET-1 and nitric oxide (NO) production in cultured placental endotheliocytes. We report that endothelial cells of arterial placental blood vessels show a dysfunctional mechanism of negative feedback regulation of ET-1 production by cGMP or insufficient NO release in response to a stimulus in the form of an increasing ET-1 concentration.

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