Carvedilol Prevents Redox Inactivation of Cardiomyocyte β1-Adrenergic Receptors

•Oxidative stress induced by acute H2O2 or chronic doxorubicin treatment leads to a decrease in β1AR expression and isoproterenol responsiveness in cardiomyocytes.•The redox-dependent disruption of the β1AR signaling pathway, which could explain the defect in catecholamine responsiveness that characteristically develops in heart failure, is prevented by the novel protein kinase C inhibitor GFX109203X or carvedilol.•Carvedilol treatment leads to the accumulation of a truncated β1AR species whose signaling properties can be distinguished from full-length β1ARs; truncated β1ARs constitutively activate protein kinase B and protect against doxorubicin-induced apoptosis.•These results identify a novel β1AR-dependent mechanism that contributes to carvedilol-induced cardioprotection.