October 27, 1998Open Access
View Full PaperReciprocal In Vivo Regulation of Myocardial G Protein–Coupled Receptor Kinase Expression by β-Adrenergic Receptor Stimulation and Blockade
Structured PICO
Does beta-adrenergic receptor stimulation or blockade alter the in vivo expression of betaARK1?
P
Population
In vivo model (specific model not detailed in abstract)
I
Intervention
Beta-adrenergic receptor (betaAR) stimulation and beta-blockade
O
Outcome
Myocardial G protein-coupled receptor kinase (betaARK1) expressionsurrogate
Demonstrates a novel mechanism of ligand-induced betaAR regulation where beta-blockade decreases betaARK1 expression, providing insight into the efficacy of beta-blockers in heart failure.
Abstract
This report demonstrates, for the first time, that betaAR stimulation can significantly increase the expression of betaARK1 , whereas beta-blockade decreases expression. This reciprocal regulation of betaARK1 documents a novel mechanism of ligand-induced betaAR regulation and provides important insights into the potential mechanisms responsible for the effectiveness of beta-blockers, such as carvedilol, in the treatment of heart failure.