Preeclampsia is a pregnancy-specific hypertensive disorder with unknown etiology, which affects 5% to 10% of all pregnancies. Increased sensitivity to the vasoconstrictor angiotensin II is a common feature of preeclampsia, although underlying mechanisms are barely understood. Recent data reveal a potential mechanism for the increased angiotensin II responsiveness in preeclampsia: increased levels of heterodimers between the vasopressor receptor AT1 and the vasodepressor receptor B2. The receptor heterodimers display increased sensitivity toward angiotensin II and are found in platelets and in omental vessels of preeclamptic women. Moreover, AT1/B2 receptor heterodimers are resistant to inactivation by reactive oxygen species, which is elevated in normal and preeclamptic pregnancies. Thus, a major symptom of preeclampsia is the result of complex formation between two G-protein-coupled receptors.