Gαi is required for carvedilol-induced β1 adrenergic receptor β-arrestin biased signaling

Abstract

β1 and β2 adrenergic receptors (ARs) are the predominant G protein-coupled receptor subtypes expressed in mammalian hearts. Here the authors describe a signaling mechanism where the biased agonist carvedilol converts β1AR from a classical Gαs-coupled to a Gαi-coupled receptor to mediate β-arrestin-dependent signaling.