LaMarca Babbette D, Ryan Michael J, Gilbert Jeffrey S, Murphy Sydney R, Granger Joey P
Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, MS 39216, USA.
Curr Hypertens Rep. 2007 Dec;9(6):480-5. doi: 10.1007/s11906-007-0088-1.
Reduced uterine perfusion pressure during pregnancy is an important initiating event in preeclampsia. Inflammatory cytokines are thought to link placental ischemia with cardiovascular and renal dysfunction. Supporting a role for cytokines are findings of elevated tumor necrosis factor (TNF)-alpha and interleukin (IL)-6 plasma levels in preeclamptic women. Blood pressure regulatory systems (eg, renin-angiotensin system [RAS] and sympathetic nervous system) interact with proinflammatory cytokines, which affect angiogenic and endothelium-derived factors regulating endothelial function. Chronic reductions in placental perfusion in pregnant rats are associated with enhanced TNF-alpha and IL-6 production. Chronic infusion of TNF-alpha or 11-6 into normal pregnant rats significantly increases arterial pressure and impairs renal hemodynamics. TNF-alpha activates the endothelin system in placental, renal, and vascular tissues, and IL-6 stimulates the RAS. These findings suggest that inflammatory cytokines elevate blood pressure during pregnancy by activating multiple neurohumoral and endothelial factors.
孕期子宫灌注压降低是先兆子痫的一个重要起始事件。炎性细胞因子被认为是胎盘缺血与心血管及肾功能障碍之间的联系纽带。先兆子痫女性体内肿瘤坏死因子（TNF）-α和白细胞介素（IL）-6血浆水平升高的研究结果支持了细胞因子的作用。血压调节系统（如肾素-血管紧张素系统[RAS]和交感神经系统）与促炎细胞因子相互作用，促炎细胞因子会影响调节内皮功能的血管生成因子和内皮源性因子。孕鼠胎盘灌注长期减少与TNF-α和IL-6生成增加有关。向正常孕鼠长期输注TNF-α或IL-6会显著升高动脉血压并损害肾血流动力学。TNF-α激活胎盘、肾脏和血管组织中的内皮素系统，而IL-6刺激RAS。这些发现表明，炎性细胞因子在孕期通过激活多种神经体液和内皮因子来升高血压。
