Current Hypertension Reports

, Volume 9, Issue 6, pp 480–485 | Cite as

Inflammatory cytokines in the pathophysiology of hypertension during preeclampsia

  • Babbette D. LaMarca
  • Michael J. Ryan
  • Jeffrey S. Gilbert
  • Sydney R. Murphy
  • Joey P. GrangerEmail author


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.


Vascular Endothelial Growth Factor Preeclampsia Preeclamptic Woman Physiol Regul Integr Comp Placental Perfusion 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.


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Copyright information

© Current Medicine Group LLC 2007

Authors and Affiliations

  • Babbette D. LaMarca
  • Michael J. Ryan
  • Jeffrey S. Gilbert
  • Sydney R. Murphy
  • Joey P. Granger
    • 1
    Email author
  1. 1.Department of Physiology and BiophysicsUniversity of Mississippi Medical CenterJacksonUSA

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