Expression of kallikrein, bradykinin b2 receptor, and endothelial nitric oxide synthase in placenta in normal gestation, preeclampsia, and placenta accreta.

In an effort to define the varied expression of three vasoactive markers in the clinical models of normal placenta/ normal invasion (n = 11), preeclampsia/restricted trophoblast invasion (n = 15), and placenta accreta/exaggerated invasion (n = 6), we performed semiquantitative immunohistochemistry for kallikrein, bradykinin B2 receptor, and endothelial nitric oxide synthase (eNOS). In the floating villi, the syncytiotrophoblast expressed more kallikrein in placenta accreta (p < 0.05), than in normal and preeclamptic placentas, while the bradykinin B2 receptor and eNOS were similarly expressed in all groups; in the fetal endothelium, the bradykinin B2 receptor was enhanced in placenta accreta (p < 0.005), but kallikrein and eNOS were similarly expressed in the other two groups. In the extravillous trophoblast, both kallikrein and eNOS expression were higher in placenta accreta (p < 0.001), while the bradykinin B2 receptor signal was only enhanced in preeclampsia (p < 0.05). The presence and localization of kallikrein, the bradykinin B2 receptor, and eNOS in the fetomaternal interface in the three study conditions supports a local role for interrelated vasodilatory/antiaggregating systems. This first report of the variations observed in kallikrein and eNOS in a condition of exaggerated trophoblast invasion supports the participation of vasodilatation in trophoblast migration.