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

超氧化物种类对先兆子痫内皮功能变化的新作用研究

基本信息

批准号：
14571578
负责人：
SUZUKI Yoshikatsu
金额：
$ 2.18万
依托单位：
Nagoya City University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2002
资助国家：
日本
起止时间：
2002 至 2003
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-14571578/
关键词：
Preeclampsia Endothelial function Superoxide

项目摘要

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.

在我们之前的研究中，发现网膜阻力动脉中内皮细胞产生的一氧化氮（NO）功能降低。其根本机制不是由 NO 的第二信使 cGMP 的产生减少而是由其下调引起（Suzuki et al.,2000）。在这项研究中，我们研究了同一动脉中其他内皮衍生舒张因子的变化，例如前列环素和内皮衍生超极化因子（EDHF）。子痫前期由于产生前列环素减少，导致内皮前列环素功能明显降低。通过使用传统的微电极技术，子痫前期的膜电位没有改变（Suzuki et al. 2002）。这些结果表明，在先兆子痫中，NO和前列环素的功能均下调，而EDHF的功能保持正常。此外，发现先兆子痫中不存在内皮细胞的形态变化(Suzuki et al.，2003)。我们利用耐硝酸甘油 (NTG) 的兔子研究了 cGMP 下调的机制。研究发现，超氧化物会降低 cGMP 的功能（Nakano et al. 2004）。将来，我们将阐明这种降低，重点关注 NTG 耐受兔和先兆子痫中阻力动脉中血管紧张素 II 1 型受体的激活导致超氧化物的增加。