Inflammatory cytokines in the pathophysiology of hypertension during preeclampsia

被引：159

作者：

LaMarca, Babbette D. ^{[1
]}

Ryan, Michael J. ^{[1
]}

Gilbert, Jeffrey S. ^{[1
]}

Murphy, Sydney R. ^{[1
]}

Granger, Joey P. ^{[1
]}

机构：

[1] Univ Mississippi, Med Ctr, Dept Physiol & Biophys, Jackson, MS 39216 USA

来源：

CURRENT HYPERTENSION REPORTS | 2007年 / 9卷 / 06期

关键词：

D O I：

10.1007/s11906-007-0088-1

中图分类号：

R6 [外科学];

学科分类号：

1002 ; 100210 ;

摘要：

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.

引用

页码：480 / 485

页数：6

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