Pathophysiology of hypertension during preeclampsia linking placental ischemia with endothelial dysfunction

被引:306
作者
Granger, JP
Alexander, BT
Llinas, MT
Bennett, WA
Khalil, RA
机构
[1] Univ Mississippi, Med Ctr, Dept Physiol, Jackson, MS 39216 USA
[2] Univ Mississippi, Med Ctr, Dept Obstet & Gynecol, Jackson, MS 39216 USA
[3] Univ Mississippi, Med Ctr, Ctr Excellence Cardiovasc Renal Res, Jackson, MS 39216 USA
关键词
kidney; pregnancy; nitric oxide; endothelin; cytokines;
D O I
10.1161/01.HYP.38.3.718
中图分类号
R6 [外科学];
学科分类号
1002 ; 100210 ;
摘要
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.
引用
收藏
页码:718 / 722
页数:5
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