Preeclampsia is defined as new onset hypertension with proteinuria during pregnancy. The initiating event in preeclampsia is postulated to be reduced uteroplacental perfusion which leads to widespread dysfunction of the maternal vascular endothelium. Inflammatory cytokines such as interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF alpha) are thought to be important links between placental ischemia and cardiovascular and renal dysfunction. Supporting a potential role of cytokines in preeclampsia are findings that plasma levels of TNF and IL-6 are elevated in women with preeclampsia. Important blood pressure regulatory systems such as the renin-angiotensin system, sympathetic nervous system, and endothelial factors interact with pro-inflammatory cytokines such as IL-6 and TNF. Pro-inflammatory cytokines also affect vascular function and endothelium-derived factors involved in blood pressure regulation. Thus, endothelial dysfunction associated with preeclampsia may be mediated by cytokines. Recent studies have indicated that chronic reductions in placental perfusion in pregnant animals are associated with enhanced production of inflammatory cytokines, such as TNF alpha and IL-6. In addition, chronic infusion of either TNF alpha or IL-6 into normal pregnant rats results in significant increases in arterial pressure and a decrease in renal hemodynamics. TNF alpha activates the endothelin system in placenta, renal and vascular tissues whereas IL-6 stimulates the renin-angiotensin system. Collectively, these findings suggest that inflammatory cytokines play a role in causing hypertension in response to chronic reductions in uterine perfusion during pregnancy by activating multiple neurohumoral and endothelial factors.
Keywords: endothelin (ET-1), IL-6, tumor necrosis factor (TNF) alpha, rennin-angiotensin system (RAS), angiotensin II
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