Inflammatory cytokines in the pathophysiology of hypertension during preeclampsia
Inflammatory cytokines in the pathophysiology of hypertension during preeclampsia
复制标题
DOI：
10.1007/s11906-007-0088-1
复制
发表时间：
2007-12-01
影响因子：
5.6
通讯作者：
Granger, Joey P.
中科院分区：
文献类型：
--
作者：
LaMarca, Babbette D.;Ryan, Michael J.;Granger, Joey P.
妊娠期间子宫灌注压降低是先兆子痫的重要始发事件。炎症细胞因子被认为将胎盘缺血与心血管和肾功能障碍联系起来。先兆子痫女性血浆肿瘤坏死因子 (TNF)-α 和白细胞介素 (IL)-6 水平升高，支持了细胞因子的作用。血压调节系统（例如肾素-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，影响调节内皮功能的血管生成和内皮衍生因子。怀孕大鼠胎盘灌注的长期减少与 TNF-α 和 IL-6 产生的增加有关。正常怀孕大鼠长期输注 TNF-α 或 IL-6 会显着增加动脉压并损害肾脏血流动力学。 TNF-α 激活胎盘、肾和血管组织中的内皮素系统，IL-6 刺激 RAS。这些发现表明，炎症细胞因子通过激活多种神经体液和内皮因子来升高妊娠期间的血压。
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 IL-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.