Background Angiotensin II type 1 receptor ( AT R) autoantibody ( AT 1- AA ) was first identified as a causative factor in preeclampsia. Unlike physiological ligand angiotensin II (Ang II ), AT 1- AA can induce vasoconstriction in a sustained manner, causing a series of adverse effects, such as vascular injury and poor placental perfusion. However, its underlying mechanisms remain unclear. Here, from the perspective of AT R internalization, the present study investigated the molecular mechanism of sustained vasoconstriction induced by AT R autoantibody. Methods and Results In the current study, we used the vascular-ring technique to determine that AT 1- AA -positive IgG, which was obtained from the sera of preeclamptic patients, induced long-term vasoconstriction in endothelium-intact or endothelium-denuded rat thoracic arteries. The effect was caused by prolonged activation of AT R downstream signals in vascular smooth muscle cells, including Ca, protein kinase C, and extracellular signal-regulated kinase 1 and 2. Then, using subcellular protein fractionation, cell surface protein biotinylation, and total internal reflection fluorescence, we found that AT 1- AA -positive IgG resulted in significantly less AT R internalization than in the Ang II treatment group. Moreover, through use of fluorescent tracing and bioluminescence resonance energy transfer, we found that AT 1- AA -positive IgG cannot induce the recruitment of β-arrestin1/2, which mediated receptor internalization. Then, the effect of sustained AT R activation induced by AT 1- AA -positive IgG was rescued by overexpression of β-arrestin2. Conclusions These data suggested that limited AT R internalization resulting from the inhibition of β-arrestin1/2 recruitment played an important role in sustained vasoconstriction induced by AT 1- AA -positive IgG, which may set the stage for avoiding AT R overactivation in the management of preeclampsia.