Myocardial oxidative stress contributes to transgenic β2-adrenoceptor activation-induced cardiomyopathy and heart failure

 2-Adrenergic Receptor Redistribution in Heart Failure Changes cAMP Compartmentation

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β-Arrestin Mediates β1-Adrenergic Receptor-Epidermal Growth Factor Receptor Interaction and Downstream Signaling

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Chronic β2-adrenoceptor stimulation impairs cardiac relaxation via reduced SR Ca2+-ATPase protein and activity

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TNF-α upregulates the A 2B adenosine receptor gene: The role of NAD(P)H oxidase 4

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Knockout of β1- and β2-adrenoceptors attenuates pressure overload-induced cardiac hypertrophy and fibrosis

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A Novel Protein Kinase A-independent, β-Arrestin-1-dependent Signaling Pathway for p38 Mitogen-activated Protein Kinase Activation by β2-Adrenergic Receptors

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Cardioprotective and Survival Benefits of Long-Term Combined Therapy with  2 Adrenoreceptor (AR) Agonist and  1 AR Blocker in Dilated Cardiomyopathy Postmyocardial Infarction

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Hematopoietic Protein Tyrosine Phosphatase Mediates  2-Adrenergic Receptor-Induced Regulation of p38 Mitogen-Activated Protein Kinase in B Lymphocytes

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Measurement of cardiac function using pressure–volume conductance catheter technique in mice and rats

(2008) Pál Pacher et al.   Nature Protocols

Mechanisms of Disease: detrimental adrenergic signaling in acute decompensated heart failure

(2008) David S Feldman et al.   Nature clinical practice. Cardiovascular medicine

Endogenous Relaxin Does Not Affect Chronic Pressure Overload-Induced Cardiac Hypertrophy and Fibrosis

(2007) Qi Xu et al.   ENDOCRINOLOGY

Cardiac implications for the use of β2-adrenoceptor agonists for the management of muscle wasting

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