Vascular Smooth Muscle Mineralocorticoid Receptor Contributes to Coronary and Left Ventricular Dysfunction After Myocardial Infarction

Mineralocorticoid receptor (MR) antagonists slow down the progression of heart failure after myocardial infarction (MI), but the cell-specific role of MR in these benefits is unclear. In this study, the role of MR expressed in vascular smooth muscle cells (VSMCs) was investigated. Two months after c...

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Veröffentlicht in:	Hypertension (Dallas, Tex. 1979) Tex. 1979), 2016-04, Vol.67 (4), p.717-723
Hauptverfasser:	Gueret, Alexandre, Harouki, Najah, Favre, Julie, Galmiche, Guillaume, Nicol, Lionel, Henry, Jean-Paul, Besnier, Marie, Thuillez, Christian, Richard, Vincent, Kolkhof, Peter, Mulder, Paul, Jaisser, Frédéric, Ouvrard-Pascaud, Antoine
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Biotechnology Cardiology and cardiovascular system Disease Models, Animal Disease Progression Heart Function Tests Human health and pathology Immunology Life Sciences Magnetic Resonance Imaging - methods Male Mice Mice, Transgenic Mineralocorticoid Receptor Antagonists - pharmacology Muscle, Smooth, Vascular - drug effects Muscle, Smooth, Vascular - metabolism Myocardial Infarction - complications Myocardial Infarction - diagnosis Naphthyridines - pharmacology Nitric Oxide - metabolism Oxidative Stress - drug effects Pharmaceutical sciences Random Allocation Receptors, Mineralocorticoid - drug effects Reference Values Risk Assessment Risk Factors Tissues and Organs Treatment Outcome Ventricular Dysfunction, Left - diagnosis Ventricular Dysfunction, Left - drug therapy Ventricular Dysfunction, Left - etiology Ventricular Remodeling - drug effects Ventricular Remodeling - physiology
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Zusammenfassung:	Mineralocorticoid receptor (MR) antagonists slow down the progression of heart failure after myocardial infarction (MI), but the cell-specific role of MR in these benefits is unclear. In this study, the role of MR expressed in vascular smooth muscle cells (VSMCs) was investigated. Two months after coronary artery ligation causing MI, mice with VSMC-specific MR deletion (MI-MR) and mice treated with the MR antagonist finerenone (MI-fine) had improved left ventricular compliance and elastance when compared with infarcted control mice (MI-CTL), as well as reduced interstitial fibrosis. Importantly, the coronary reserve assessed by magnetic resonance imaging was preserved (difference in myocardial perfusion before and after induction of vasodilatation, mL mg minMI-CTL1.1±0.5, nonsignificant; MI-MR4.6±1.6 [P
ISSN:	0194-911X 1524-4563
DOI:	10.1161/HYPERTENSIONAHA.115.06709