The study for novel effects of superoxide species on changes in endothelial function in preeclampsia

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In our previous study, the reduced function of nitric oxide (NO) produced by endothelial cells was found in omental resistance arteries. The underlying mechanism was caused by not reduced production but down-regulation of cGMP, the 2nd messenger of NO (Suzuki et al.,2000).In this study, we investigated the changes in other endothelium derived relaxing factors, such as prostacyclin and endothelium-derived hyperpolarizing factor (EDHF) in same artery. The reduced function of endothelial prostacyclin was obvious due to the reduction of producing prostacyclin in preeclampsia. By use of conventional microelectrode technique, the membrane potential was not changed in preeclampsia (Suzuki et al. 2002). These results suggested that in preeclampsia, the function not only of NO but also prostacyclin is down-regulated, while the function of EDHF remains normal. Furthermore, it was found that the morphological change in endothelial cell is not present in preeclampsia (Suzuki et al.,2003). We investigated the mechanism of down-regulation of cGMP by use of nitoriglycerin (NTG)-tolerant rabbit. It was found that the function of cGMP is reduced by superoxide (Nakano et al. 2004).In the future, we will clarify with this reduction, focusing on the increase in superoxide via activation of angiotensin II type 1 receptor in resistance artery in both NTG-tolerant rabbit and preeclampsia.