Disturbed nitric oxide/endothelin-1 equilibrium in cultured human placental endotheliocytes in preeclampsia.
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.
Leszczyńska-Gorzelak
B
B
Department of Obstetrics and Perinatology, Medical Academy of Lublin, Poland.
Oleszczuk
J
J
Kamiński
K
K
Szymula
D
D
Gorzelak
M
M
Oleszczuk
J J
JJ
D002478:Cells, Cultured; D003470:Culture Media; D006152:Cyclic GMP / Q000494:pharmacology; D019332:Endothelin-1 / Q000378:metabolism*; D004730:Endothelium, Vascular / Q000187:drug effects / Q000378:metabolism*; D005246:Feedback; D005260:Female; D006801:Humans; D009569:Nitric Oxide / Q000378:metabolism*; D010920:Placenta / Q000098:blood supply*; D011225:Pre-Eclampsia / Q000378:metabolism*; D011247:Pregnancy
D003470:Culture Media; D019332:Endothelin-1; D009569:Nitric Oxide; D006152:Cyclic GMP