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功能性证据表明,人类胎盘血管中存在对氧敏感的电压门控钾通道。

Functional evidence for oxygen-sensitive voltage-gated potassium channels in human placental vasculature.

机构信息

Maternal and Fetal Health Research Centre, School of Biomedicine, The University of Manchester, 5th Floor (Research), St. Mary's Hospital, Manchester, UK.

出版信息

Placenta. 2010 Jun;31(6):553-5. doi: 10.1016/j.placenta.2010.03.009. Epub 2010 May 6.

Abstract

Hypoxic fetoplacental vasoconstriction (HFPV), involving voltage-gated potassium (K(V)) channels, has been suggested in human placenta; the identity of these channels remains unclear. Using wire myography, chorionic plate blood vessels were exposed to isoform-specific K(V) channel blockers. Dose-response curves (thromboxane mimetic U46619; 0.1-2000 nM) pre- and post-addition of K(V) channel modulator were analysed. Arterial U46619-induced contraction increased with margatoxin and stromatoxin-1, whilst only correolide increased U46619-induced contraction in veins (P < 0.05 two-way ANOVA). Basal tone was unaffected in arteries or veins. These data implicate K(V)1.2 and/or K(V)2.1 and K(V)1.5 in the control of agonist-induced contraction of human placental arteries and veins respectively.

摘要

缺氧性胎-胎盘血管收缩(HFPV)涉及电压门控钾(K(V))通道,已在人胎盘内提出;这些通道的身份仍不清楚。使用线描记法,绒毛板血管暴露于同工型特异性 K(V)通道阻滞剂。分析了 K(V)通道调节剂加入前后的剂量反应曲线(血栓烷模拟物 U46619;0.1-2000 nM)。动脉 U46619 诱导的收缩随着 margatoxin 和 stromatoxin-1 而增加,而只有 correolide 增加了静脉中 U46619 诱导的收缩(P < 0.05 双向 ANOVA)。动脉或静脉的基础张力不受影响。这些数据表明 K(V)1.2 和/或 K(V)2.1 和 K(V)1.5 分别控制人胎盘动脉和静脉中激动剂诱导的收缩。

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