Prostaglandin I2 mediates weak vasodilatation in human placental microvessels
Prostaglandin I2 mediates weak vasodilatation in human placental microvessels
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DOI：
10.1093/biolre/ioaa156
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发表时间：
2020-09
影响因子：
3.6
通讯作者：
Xueqin Feng;Yingying Zhang;Yumeng Zhang;Xiaojun Yang;Dongmei Man;Likui Lu;Ting Xu;Yanping Liu;Chunli Yang;Huan Li;Linglu Qi;Hongyu Su;Xiuwen Zhou;Zhice Xu
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文献类型：
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作者：
Xueqin Feng;Yingying Zhang;Yumeng Zhang;Xiaojun Yang;Dongmei Man;Likui Lu;Ting Xu;Yanping Liu;Chunli Yang;Huan Li;Linglu Qi;Hongyu Su;Xiuwen Zhou;Zhice Xu
摘要人胎盘血管在母胎循环中起着重要的代谢物和氧交换作用。内皮源性前列环素（前列腺素I2，PGI 2）是体内重要的内皮血管扩张剂。然而，内皮细胞PGI 2在人胎盘中的生理和药理学功能仍不清楚。本研究中使用了人、绵羊和大鼠血管。与非胎盘血管（非肺静脉），PGI 2合成抑制剂反苯环丙胺（TCP）没有修改5-羟色胺（5-HT）诱导的血管收缩，表明内皮源性PGI 2是弱的肺静脉。血管对外源性PGI 2的反应表现出轻微的舒张，随后在HPV中在较高浓度下显著收缩，这被血栓烷-前列腺素（TP）受体拮抗剂SQ-29，548抑制。来自绵羊的PV和非PV的测试也显示出类似的功能结果。HPV的TP受体多于PGI_2（IP）受体。HPV的全细胞K+电流密度明显弱于非PVs。本研究证明了胎盘内源性内皮PGI 2系统的特定特征和胎盘血管对外源性PGI 2的生理/药理学反应模式，表明胎盘内皮PGI 2对人胎盘血管扩张无显著作用，与非PV形成显著对比。这些结果为理解HPV的内皮作用提供了重要信息，这可能有助于进一步研究治疗疾病（如先兆子痫）的潜在靶点。PGI 2对人胎盘血管扩张无明显作用，这为了解胎盘中内皮的作用提供了重要信息，并为研究抗先兆子痫的潜在靶点提供了新的见解。
Abstract 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. Summary sentence PGI2 dose not markedly contribute to vascular dilation in the human placenta, providing crucial information for understanding the endothelial roles in the placenta, and offering new insights into investigations of potential targets against preeclampsia.