Women who have had preeclampsia have increased CVD risk, however the mechanism(s) responsible for this association remain unclear. Microvascular damage sustained during a preeclamptic pregnancy may persist post-partum. The putative mechanisms mediating this dysfunction include a reduction in nitric oxide (NO)-dependent dilation, and an increased sensitivity to angiotensin II (ang II). In this study, we evaluated endothelium-dependent dilation, ang II sensitivity, and the therapeutic effect of ang II receptor blockade (losartan) on endothelium-dependent dilation in vivo in the microvasculature of women with a history of preeclampsia (PrEC, n=12) and control women who had a healthy pregnancy (HC, n=12). We hypothesized that PrEC would have 1) reduced endothelium-dependent dilation, 2) reduced NO-mediated dilation, and 3) increased sensitivity to ang II. We further hypothesized that localized losartan would increase endothelium-dependent vasodilation in PrEC. We assessed microvascular endothelium-dependent vasodilator function by measurement of cutaneous vascular conductance responses to graded infusion of acetylcholine (ACh; 10−7–102mmol/L) and a standardized local heating protocol in control sites and sites treated with 15mmol/L L-NAME (NO-synthase inhibitor) or 43μmol/L losartan. Further, we assessed microvascular vasoconstrictor sensitivity to ang II (10−20–10−4mol/L). PrEC had significantly reduced endothelium-dependent dilation (−0.3±0.5 vs −1.0±0.4 logEC50; P<0.001) and NO-dependent dilation (16±3 vs 39±6%; P=0.006). PrEC also had augmented vasoconstrictor sensitivity to ang II (−10.2±1.3 vs −8.3±0.5; P=0.006). AT1R-inhibition augmented endothelium-dependent vasodilation and NO-dependent dilation in PrEC but had no effect in HC. These data suggest that women who have had preeclampsia have persistent microvascular dysfunction post-partum, mediated in part by increased sensitivity to ang II.