Jakoubek V, Bíbová J, Hampl V
Department of Physiology, Charles University Second Medical School, Prague, Czech Republic.
Placenta. 2006 Sep-Oct;27(9-10):1030-3. doi: 10.1016/j.placenta.2005.10.006. Epub 2005 Dec 20.
Unlike all vascular beds with the exception of the pulmonary circulation, fetoplacental vessels respond to acute hypoxia with vasoconstriction. While this hypoxic fetoplacental vasoconstriction (HFPV) is considered essential in the pathogenesis of intrauterine growth retardation, its mechanism is largely unknown. Hypoxia inhibits potassium channels and thus causes depolarization in fetoplacental vascular smooth muscle. We propose that this hypoxia-induced depolarization leads to vasoconstriction by activating voltage-dependent calcium (Ca) channels and Ca influx. We compared HFPV between isolated perfused human cotyledons treated with an inhibitor of L-type channels, nifedipine, and preparations receiving only vehicle. While the solvent (diluted DMSO) had no inhibitory effect on HFPV, the hypoxic responses were completely abolished even by a relatively low dose of nifedipine (1 nM). We conclude that activation of L-type Ca channels is an essential part of HFPV.
除肺循环外，与所有血管床不同，胎儿胎盘血管对急性缺氧的反应是血管收缩。虽然这种缺氧性胎儿胎盘血管收缩（HFPV）被认为是宫内生长迟缓发病机制中的关键因素，但其机制在很大程度上尚不清楚。缺氧会抑制钾通道，从而导致胎儿胎盘血管平滑肌去极化。我们认为，这种缺氧诱导的去极化通过激活电压依赖性钙（Ca）通道和Ca内流导致血管收缩。我们比较了用L型通道抑制剂硝苯地平处理的离体灌注人胎盘小叶与仅接受赋形剂的制剂之间的HFPV。虽然溶剂（稀释的二甲亚砜）对HFPV没有抑制作用，但即使是相对低剂量的硝苯地平（1 nM）也能完全消除缺氧反应。我们得出结论，L型钙通道的激活是HFPV的重要组成部分。
