当前位置: X-MOL 学术Biol. Reprod. › 论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
Prostaglandin I2 Mediates Weak Vasodilatation in Human Placental Microvessels†.
Biology of Reproduction ( IF 3.1 ) Pub Date : 2020-09-09 , DOI: 10.1093/biolre/ioaa156
Xueqin Feng 1, 2 , Yingying Zhang 1 , Yumeng Zhang 1 , Xiaojun Yang 3 , Dongmei Man 2 , Likui Lu 1 , Ting Xu 1 , Yanping Liu 1 , Chunli Yang 1 , Huan Li 1 , Linglu Qi 1 , Hongyu Su 1 , Xiuwen Zhou 1 , Zhice Xu 1
Affiliation  

Human placental vessels (HPVs) play important roles in the exchange of metabolites and oxygen in maternal-fetal circulation. Endothelial-derived prostacyclin (prostaglandin I2, PGI2) is a critical endothelial vasodilator in the body. However, the physiological and pharmacological functions of endothelial PGI2 in the human placenta are still unclear. Human, sheep, and rat blood vessels were used in this study. Unlike non-placental vessels (non-PVs), the PGI2 synthesis inhibitor tranylcypromine (TCP) did not modify 5-hydroxytryptamine (5-HT)-induced vascular contraction, indicating that endothelial-derived PGI2 was weak in PVs. Vascular responses to exogenous PGI2 showed slight relaxation followed by a significant contraction at a higher concentration in HPV, which was inhibited by the thromboxane-prostanoid (TP) receptors antagonist SQ-29,548. Testing PVs and non-PVs from sheep also showed similar functional results. More TP receptors than PGI2 (IP) receptors were observed in HPVs. The whole-cell K+ current density of HPVs was significantly weaker than that of non-PVs. This study demonstrated the specific characteristics of the placental endogenous endothelial PGI2 system and the patterns of placental vascular physiological/pharmacological response to exogenous PGI2, showing that placental endothelial PGI2 does not markedly contribute to vascular dilation in the human placenta, in notable contrast to non-PVs. The results provide crucial information for understanding the endothelial roles of HPVs, which may be helpful for further investigations of potential targets in the treatment of diseases such as preeclampsia.

中文翻译:

前列腺素 I2 介导人胎盘微血管中的弱血管舒张†。

人胎盘血管 (HPV) 在母胎循环中代谢物和氧气的交换中起着重要作用。内皮衍生的前列环素(前列腺素 I 2,PGI 2)是体内重要的内皮血管扩张剂。然而,内皮PGI 2在人胎盘中的生理和药理功能仍不清楚。本研究中使用了人类、绵羊和大鼠血管。与非胎盘血管 (non-PVs) 不同,PGI 2合成抑制剂反苯环丙胺 (TCP) 不会改变 5-羟色胺 (5-HT) 诱导的血管收缩,表明内皮衍生的 PGI 2在 PVs 中较弱。对外源性 PGI 2 的血管反应在较高浓度的 HPV 中显示轻微松弛,然后显着收缩,这被血栓素 - 前列腺素 (TP) 受体拮抗剂 SQ-29,548 抑制。测试来自绵羊的 PV 和非 PV 也显示了类似的功能结果。在 HPV 中观察到的TP 受体多于 PGI 2 (IP) 受体。HPVs的全细胞 K +电流密度明显低于非 PVs。本研究证明了胎盘内源性内皮 PGI 2系统的具体特征和胎盘血管对外源性 PGI 2 的生理/药理反应模式表明胎盘内皮 PGI 2与非 PVs 形成显着对比,在人胎盘中不会显着促进血管扩张。该结果为了解 HPV 的内皮作用提供了关键信息,这可能有助于进一步研究治疗先兆子痫等疾病的潜在靶点。
更新日期:2020-09-09
down
wechat
bug