Title |
ACE-inhibition, but not weight reduction restores cardiomyocyte response to β-adrenergic stimulation in the metabolic syndrome
|
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Published in |
BMC Cardiovascular Disorders, July 2013
|
DOI | 10.1186/1471-2261-13-51 |
Pubmed ID | |
Authors |
Ines Nevelsteen, Virginie Bito, Gerry Van der Mieren, Annelies Vanderper, An Van den Bergh, Karin R Sipido, Kanigula Mubagwa, Paul Herijgers |
Abstract |
Diabetic cardiomyopathy is characterized by systolic and early diastolic ventricular dysfunction. In the metabolic syndrome (MS), ventricular stiffness is additionally increased in a later stage. It is unknown whether this is related to intrinsic cardiomyocyte dysfunction, extrinsic factors influencing cardiomyocyte contractility and/or cardiac function, or a combination of both. A first aim was to study cardiomyocyte contractility and Ca2+ handling in vitro in a mouse model of MS. A second aim was to investigate whether in vivo hypocaloric diet or ACE-inhibition (ACE-I) improved cardiomyocyte contractility in vitro, contractile reserve and Ca2+ handling. |
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Mendeley readers
Geographical breakdown
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Unknown | 35 | 95% |
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Unknown | 10 | 27% |
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