Department of Surgery, The University of Mississippi Medical Center, Jackson, Mississippi, USA.
J Hypertens. 2019 Mar;37(3):476-487. doi: 10.1097/HJH.0000000000001901.
: Proper vascular tone and blood pressure regulation during pregnancy are important for immediate and long-term cardiovascular health of the mother and her offspring. Preeclampsia is clinically defined as new-onset maternal hypertension accompanied by cardiovascular, renal, and/or neural abnormalities presenting in the second half of pregnancy. There is strong evidence to support that preeclampsia is mediated by attenuations in uteroplacental vascular remodeling and increases in vasoconstriction with subsequent placental ischemia/reperfusion-induced release of hypertensive substances into the maternal circulation. These include antiangiogenic and pro-inflammatory factors. There is also evidence implicating increased sympathetic nervous system activity (SNA) in this maternal disorder, but this mostly includes data correlating severity of disease with catecholamine levels and elevated muscle SNA. These measurements have not confirmed a causative role for SNA in the pathogenesis of preeclampsia. Therefore, studies are needed to provide a comprehensive understanding of SNA and its control of vascular function and blood pressure regulation during normal pregnancy in order to set the stage for exploring the mechanisms mediating the exaggerated SNA and signaling during preeclampsia. This review examines the role of SNA in control of uteroplacental vascular tone and blood pressure regulation during normal pregnancy. Furthermore, it is proposed that over-activation of the SNA contributes to altered uteroplacental vascular tone and perfusion leading to placental ischemic events and modulates the systemic vasoconstriction and hypertensive responses to soluble placenta ischemic factors. Recognizing the integrative role and importance of SNA in the pathophysiology of preeclampsia will advance our understanding of this maternal disorder.
在怀孕期间保持适当的血管张力和血压调节对于母亲及其后代的即时和长期心血管健康非常重要。子痫前期的临床定义为妊娠后半期新出现的母体高血压，并伴有心血管、肾脏和/或神经异常。有强有力的证据表明，子痫前期是由胎盘血管重塑减弱和血管收缩增加引起的，随后胎盘缺血/再灌注导致高血压物质释放到母体循环中。这些物质包括抗血管生成和促炎因子。也有证据表明，在这种母体疾病中，交感神经系统活动（SNA）增加，但这些数据主要包括将疾病严重程度与儿茶酚胺水平和升高的肌肉 SNA 相关联的数据。这些测量并没有证实 SNA 在子痫前期发病机制中的因果作用。因此，需要进行研究，以全面了解 SNA 及其对正常妊娠期间血管功能和血压调节的控制，以便为探索介导子痫前期中 SNA 及其信号的过度激活的机制奠定基础。本综述探讨了 SNA 在正常妊娠期间控制胎盘血管张力和血压调节中的作用。此外，有人提出，SNA 的过度激活会导致胎盘血管张力和灌注改变，导致胎盘缺血事件，并调节全身血管收缩和对可溶性胎盘缺血因子的高血压反应。认识到 SNA 在子痫前期病理生理学中的整合作用和重要性将促进我们对这种母体疾病的理解。
