Maternal and Fetal Health Research Centre, School of Biomedicine, The University of Manchester, 5th Floor (Research), St. Mary's Hospital, Manchester, UK.
Placenta. 2010 Jun;31(6):553-5. doi: 10.1016/j.placenta.2010.03.009. Epub 2010 May 6.
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.
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。
