Carvedilol Prevents Redox Inactivation of Cardiomyocyte Β₁-Adrenergic Receptors.

ABSTRACT: The mechanism that leads to a decrease in β₁-adrenergic receptor (β₁AR) expression in the failing heart remains uncertain. This study shows that cardiomyocyte β₁AR expression and isoproterenol responsiveness decrease in response to oxidative stress. Studies of mechanisms show that the redox-dependent decrease in β₁AR expression is uniquely prevented by carvedilol and not other βAR ligands. Carvedilol also promotes the accumulation of N-terminally truncated β₁ARs that confer protection against doxorubicin-induced apoptosis in association with activation of protein kinase B. The redox-induced molecular controls for cardiomyocyte β₁ARs and pharmacologic properties of carvedilol identified in this study have important clinical a

SUBMITTER: Park M 

PROVIDER: S-EPMC6116783 | biostudies-literature | 2018 Aug

REPOSITORIES: biostudies-literature