Fig. 5.

Schematic representation of the mechanisms contributing to microvascular dysfunction in women who have had preeclampsia. An increase in angiotensin II (ANG II) sensitivity and increased endothelin-1 (ET-1) production, coupled with attenuated ET-1-mediated vasodilation, result in persistent vascular smooth muscle vasoconstriction and attenuated vasodilation responses to endothelium-dependent agonists. AT₁R, ANG II type 1 receptor; TNF-α, tumor necrosis factor-α; ET_AR, endothelin receptor type A; ET_BR, endothelin receptor type B; M, membrane-bound receptor; NO, nitric oxide.