Inflammatory cytokines in the pathophysiology of hypertension during preeclampsia

Babbette D. LaMarca, Michael J. Ryan, Jeff Gilbert, Sydney R. Murphy, Joey P. Granger

Research output: Contribution to journalReview articlepeer-review

140 Scopus citations

Abstract

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)-α 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-α and IL-6 production. Chronic infusion of TNF-α or IL-6 into normal pregnant rats significantly increases arterial pressure and impairs renal hemodynamics. TNF-α 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.

Original languageEnglish (US)
Pages (from-to)480-485
Number of pages6
JournalCurrent Hypertension Reports
Volume9
Issue number6
DOIs
StatePublished - Dec 1 2007

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