β-Adrenergic receptor kinase-1 levels in catecholamine-induced myocardial hypertrophy: Regulation by β- but not α1-adrenergic stimulation

Guido Iaccarino, Paul C. Dolber, Robert J. Lefkowitz, Walter J. Koch

    Research output: Contribution to journalArticle

    69 Scopus citations

    Abstract

    Pressure overload ventricular hypertrophy is accompanied by dysfunctional β-adrenergic receptor signaling due to increased levels of the β-adrenergic receptor kinase-1, which phosphorylates and desensitizes β- adrenergic receptors. In this study, we examined whether increased β- adrenergic receptor kinase 1 expression is associated with myocardial hypertrophy induced by adrenergic stimulation. With use of implanted mini- osmotic pumps, we treated mice with isoproterenol, phenylephrine, or vehicle to distinguish between α1- and β-adrenergic stimulation. Both treatments resulted in cardiac hypertrophy, but only isoproterenol induced significant increases in β-adrenergic receptor kinase-1 protein levels and activity. Similarly, in isolated adult rat cardiac myocytes, 24 hours of isoproterenol stimulation resulted in a significant 2.8-fold increase in β-adrenergic receptor kinase-1 protein levels, whereas 24 hours of phenylephrine treatment did not alter β-adrenergic receptor kinase-1 expression. Our results indicate that increased β-adrenergic receptor kinase-1 is not invariably associated with myocardial hypertrophy but apparently is controlled by the state of β-adrenergic receptor activation.

    Original languageEnglish (US)
    Pages (from-to)396-401
    Number of pages6
    JournalHypertension
    Volume33
    Issue number1 II
    StatePublished - Jan 1 1999

    Keywords

    • Catecholamines
    • Desensitization
    • G protein-coupled receptor kinases
    • Myocardial hypertrophy
    • β-Adrenergic receptor

    ASJC Scopus subject areas

    • Internal Medicine

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