Previously, we demonstrated activation of the renin angiotensin system (RAS) in the fetal placental chorionic villi, but it is unknown if the immediately adjacent area of the maternal uterine placental bed is regulated similarly. This study measured angiotensin peptides, RAS component mRNAs, and receptor binding in the fundus from non-pregnant subjects (n=19) and in the uterine placental bed from normal (n=20) and preeclamptic (n=14) subjects. In the uterine placental bed from normal pregnant women, angiotensin II peptide levels and angiotensinogen, angiotensin converting enzyme, AT₁, AT₂, and Mas mRNA expression were lower as compared with the non-pregnant subjects. In preeclamptic uterine placental bed, angiotensin II peptide levels and renin and angiotensin converting enzyme mRNA expression were significantly higher than normal pregnant subjects. The AT₂ receptor was the predominant receptor subtype in the non-pregnant fundus, while all angiotensin receptor binding was undetectable in normal and preeclamptic pregnant uterine placental bed compared to non-pregnant fundus. These findings suggest that the maternal uterine placental bed may play an endocrine role by producing Ang II and its acting in the adjacent placenta to vasoconstrict fetal chorionic villi vessels where we have shown previously that AT₁ receptors predominate. This would lead to decreased maternal-fetal oxygen exchange and fetal nutrition, a known characteristic of preeclampsia.