NITRIC-OXIDE PRODUCTION BY HUMAN UMBILICAL VESSELS IN SEVERE PREECLAMPSIA

Objective: Pre-eclampsia is characterized by an increased vascular ton e which might be related to an abnormal endothelial cell function. As representatives of the fetal circulation, we compared the nitric oxide (NO)-releasing capacity of human umbilical vessels from normal and pr e-eclamptic pregnancies. Methods: Normal and pre-eclamptic umbilical v essels were mounted in parallel in an organ chamber with three perfusi on lines superfusing the same detector tissue (rubbed rat aortic ring) . In this cascade system the capacity of the umbilical vessels to rele ase NO was measured under basal conditions and after stimulation with histamine, bradykinin or calcium ionophore A23187. Results: Relaxation s dependent on basal NO release were found to be significantly higher in pre-eclamptic vessels (especially in veins) than in normal vessels. Conversely, stimulated NO release in response to histamine or bradyki nin was significantly decreased in pre-eclamptic umbilical arteries, b ut not in veins, compared with normal vessels. However, there was no s ignificant difference in the release of NO in response to A23187 betwe en normal and pre-eclamptic vessels. Conclusions: The NO-releasing and NO-producing capacity in the vessels from fetal circulation is not di minished in pre-eclampsia. However, in pre-eclamptic umbilical arterie s the NO release in response to certain stimuli (histamine or bradykin in) is diminished, probably as a result of alterations in the receptor function.