Figure 1.

The AT1R-B2R protein complex forms a platform for enhanced G-protein activation. The scheme illustrates how protein complex formation between AT1R (angiotensin II receptor type 1) and B2R (bradykinin B2 receptor) facilitates the interaction with heterotrimeric G-proteins such as Gq/11 (heterotrimeric GTP-binding protein of Gq/11 family) and Gi/o (heterotrimeric GTP-binding protein of Gi/o family). As a consequence of stabilized G-protein interaction, stimulation of the AT1R-B2R protein complex with angiotensin II (AngII) or mechanical stimulation leads to enhanced G-protein activation and signaling, and beta-arrestin1 (ARRB1) dysfunction (right side) compared to the monomeric AT1 receptor (left side). This Figure was adapted from [90].