Abstract
The influence of bradykinin (BK) on the production of prostacyclin and thromboxane was investigated by in vitro perfusion of umbilical arteries from normal pregnancies and from pregnancies complicated by preeclampsia. The production of prostacyclin was significantly lower and that of thromboxane significantly higher in the preeclampsia group than in the normotensive group. BK stimulated the prostacyclin formation, being more potent in the normotensive group as compared to the preeclampsia group. As for thromboxane, BK caused a dose-dependent increase in the preeclampsia group and a decrease in the control group. By employing specific BK-agonists/-antagonists the stimulatory effect of BK was found to be mediated by B2-receptors. The results indicate changes in the interaction of the kinin-kallikrein and prostanoid systems in the fetal circulation in preeclampsia.