Abstract
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.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
