Granger J P, Alexander B T, Llinas M T, Bennett W A, Khalil R A
Department of Physiology, Center for Excellence in Cardiovascular-Renal Research, University of Mississippi Medical Center, Jackson, USA.
Hypertension. 2001 Sep;38(3 Pt 2):718-22. doi: 10.1161/01.hyp.38.3.718.
Studies over the past decade have provided a better understanding of the potential mechanisms responsible for the pathogenesis of preeclampsia. The initiating event in preeclampsia has been postulated to be reduced uteroplacental perfusion as a result of abnormal cytotrophoblast invasion of spiral arterioles. Placental ischemia is thought to lead to widespread activation/dysfunction of the maternal vascular endothelium that results in enhanced formation of endothelin and thromboxane, increased vascular sensitivity to angiotensin II, and decreased formation of vasodilators such as NO and prostacyclin. These endothelial abnormalities, in turn, cause hypertension by impairing renal-pressure natriuresis and increasing total peripheral resistance. The quantitative importance of the various endothelial and humoral factors in mediating the reduction in renal hemodynamic and excretory function and elevation in arterial pressure during preeclampsia are still unclear. Results from ongoing basic and clinical studies, however, should provide new and important information regarding the physiological mechanisms responsible for the elevation in arterial pressure in women with preeclampsia.
过去十年的研究使人们对先兆子痫发病机制的潜在机制有了更好的理解。先兆子痫的起始事件被推测为由于细胞滋养层对螺旋小动脉的异常侵袭导致子宫胎盘灌注减少。胎盘缺血被认为会导致母体血管内皮广泛激活/功能障碍，从而导致内皮素和血栓素形成增加、血管对血管紧张素II的敏感性增加以及血管舒张剂如一氧化氮和前列环素的形成减少。这些内皮异常继而通过损害肾压力利尿和增加总外周阻力导致高血压。在先兆子痫期间，各种内皮和体液因素在介导肾血流动力学和排泄功能降低以及动脉压升高方面的定量重要性仍不清楚。然而，正在进行的基础和临床研究结果应该会提供有关先兆子痫女性动脉压升高的生理机制的新的重要信息。
