Angiotensin II (AngII) interacts with two receptor subtypes, AT₁ and AT₂, belonging to the seven transmembrane receptor superfamily. Pharmacological investigations initially suggested that AT₂ receptors antagonize AT₁ effects. Data from AT₂ receptor transgenic and knock-out mice have not been entirely consistent with this interpretation. At the cellular level, a clear mechanistic model of AT₂ transduction and signalling has yet to emerge. The AT₂ receptor displays the hallmark motifs and signature residues of a G protein-coupled receptor (GPCR), but fails to demonstrate most of the classic features of GPCR signalling. In recent years, unbiased screens for AT₂-interacting proteins have identified novel partner proteins involved in AT₂ signalling, providing new insight into the mechanisms of AT₂ action. A growing body of evidence suggests that the AT₂ receptor is constitutively active (i.e. signals without AngII). This review critically evaluates controversies surrounding physiological functions and signalling mechanisms of the AT₂ receptor, primarily in a cardiovascular context. Recent advances in the field are highlighted and findings challenging the concept that the AT₂ receptor is a conventional angiotensin receptor are considered.