Several examples of functional G-protein–coupled receptor heterodimers have been identified. However, it is not known whether receptor heterodimerization is involved in the pathogenesis of human disorders. Here we show that in preeclamptic hypertensive women, a significant increase in heterodimerization occurs between the AT₁-receptor for the vasopressor angiotensin II and the B₂-receptor for the vasodepressor bradykinin. AT₁–B₂-receptor heterodimerization in preeclampsia correlated with a 4–5-fold increase in B₂-receptor protein levels. Expression of the AT₁–B₂ heterodimer increased the responsiveness to angiotensin II and conferred resistance in AT₁-receptors to inactivation by reactive oxygen species raised in normotensive and preeclamptic pregnancies. We suggest that AT₁–B₂ heterodimers contribute to angiotensin II hypersensitivity in preeclampsia. Moreover, we identify preeclampsia as the first disorder associated with altered G-protein–coupled receptor heterodimerization.