Accumulation of pathological AT1R-B2R aggregates during the pathogenesis of preeclampsia. Pregnancy-induced inflammation triggers AT1R-B2R protein complexes in individuals with major risk factors of preeclampsia and vascular dysfunction. AT1R-B2R stimulates enhanced calcium signaling, aggravates vascular dysfunction and promotes accumulation of pathological AT1R-B2R protein aggregates, in part by ARRB1 dysfunction. At later stages of pregnancy, when mechanical forces are high, pathological AT1R-B2R protein complexes are activated by mechanical forces without angiotensin II, trigger agonistic AT1R autoantibodies and symptoms of preeclampsia.