Carvedilol Prevents Redox Inactivation of Cardiomyocyte ?1-Adrenergic Receptors.
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ABSTRACT: The mechanism that leads to a decrease in ?1-adrenergic receptor (?1AR) expression in the failing heart remains uncertain. This study shows that cardiomyocyte ?1AR expression and isoproterenol responsiveness decrease in response to oxidative stress. Studies of mechanisms show that the redox-dependent decrease in ?1AR expression is uniquely prevented by carvedilol and not other ?AR ligands. Carvedilol also promotes the accumulation of N-terminally truncated ?1ARs that confer protection against doxorubicin-induced apoptosis in association with activation of protein kinase B. The redox-induced molecular controls for cardiomyocyte ?1ARs and pharmacologic properties of carvedilol identified in this study have important clinical and therapeutic implications.
SUBMITTER: Park M
PROVIDER: S-EPMC6116783 | biostudies-literature |
REPOSITORIES: biostudies-literature
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