Dual agonist occupancy of AT1-R-α2C-AR heterodimers results in atypical Gs-PKA signaling.

Technologies that bias GPCR expression for formation of heterodimers show that, when heterodimerized, α2C-AR and AT-1R exhibit atypical Gs-cAMP-PKA signaling upon ligand stimulation compared to either parent receptor expressed alone and mimic activation associated with arterial hypertension.