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Beta3-adrenergic eNOS stimulation in left ventricular murine myocardium
Klara Brixius1, Wilhelm Bloch, Christoph Ziskoven
1Laboratory of Muscle Research and Molecular Cardiology, Department of Internal Medicine III, University of Cologne, Germany.
Canadian Journal of Physiology and Pharmacology
|March 3, 2007
Summary
Beta3-adrenergic activation stimulates nitric oxide (NO) release via endothelial nitric oxide synthase (eNOS) in mouse heart. These pathways are region-specific and may involve free radical production in heart failure.
Area of Science:
- Cardiovascular Physiology
- Molecular Cardiology
- Adrenergic Signaling
Background:
- Beta3-adrenergic receptors play a role in cardiac function.
- Endothelial nitric oxide synthase (eNOS) regulates vascular tone and cardiac function.
- Understanding beta3-adrenergic modulation of eNOS is crucial for cardiovascular health.
Purpose of the Study:
- To investigate the mechanisms of beta3-adrenergic activation of eNOS in mouse myocardium.
- To determine the role of beta3-adrenoceptors in nitric oxide (NO) liberation and eNOS phosphorylation.
- To explore regional differences in eNOS activation pathways within the heart.
Main Methods:
- Utilized wild-type (WT) and beta3-adrenoceptor knockout (beta3-KNO) mice.
- Measured NO release using diaminofluorescein (DAF) fluorescence.
- Assessed eNOS phosphorylation (Ser1177, Thr495, Ser114) and translocation via immunohistochemistry.
- Quantified 8-isoprostaglandin F2alpha as a marker for reactive oxygen species.
Main Results:
- Beta3-adrenergic agonist BRL 37344 increased NO release in WT mouse atria and ventricles, but not in beta3-KNO mice.
- NO liberation was associated with increased eNOSSer1177 phosphorylation in WT mice.
- Cytosolic eNOS translocation occurred in the right atrium, while eNOSSer114 phosphorylation increased in the left ventricle, paralleled by elevated 8-isoprostaglandin F2alpha.
Conclusions:
- Two distinct beta3-adrenoceptor-dependent pathways activate eNOS: phosphorylation of Ser1177 and Ser114, and translocation.
- These activation pathways are utilized in a region-dependent manner within the murine myocardium.
- Beta3-adrenergic-mediated oxygen-derived free radical production may be significant during heightened receptor activation, relevant to human heart failure.
