Ranolazine prevents INaL enhancement and blunts myocardial remodelling in a model of pulmonary hypertension

Pulmonary arterial hypertension (PAH) reflects abnormal pulmonary vascular resistance and causes right ventricular (RV) hypertrophy. Enhancement of the late sodium current (INaL) may result from hypertrophic remodelling. The study tests whether: (i) constitutive INaL enhancement may occur as part of...

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Veröffentlicht in:	Cardiovascular research 2014-10, Vol.104 (1), p.37-48
Hauptverfasser:	Rocchetti, Marcella, Sala, Luca, Rizzetto, Riccardo, Staszewsky, Lidia Irene, Alemanni, Matteo, Zambelli, Vanessa, Russo, Ilaria, Barile, Lucio, Cornaghi, Laura, Altomare, Claudia, Ronchi, Carlotta, Mostacciuolo, Gaspare, Lucchetti, Jacopo, Gobbi, Marco, Latini, Roberto, Zaza, Antonio
Format:	Artikel
Sprache:	eng
Schlagworte:	Acetanilides - pharmacology Animals Calcium Signaling - drug effects Collagen - metabolism Disease Models, Animal Fibrosis Hypertension, Pulmonary - chemically induced Hypertension, Pulmonary - drug therapy Hypertension, Pulmonary - metabolism Hypertension, Pulmonary - pathology Hypertension, Pulmonary - physiopathology Hypertrophy, Right Ventricular - etiology Hypertrophy, Right Ventricular - metabolism Hypertrophy, Right Ventricular - pathology Hypertrophy, Right Ventricular - physiopathology Hypertrophy, Right Ventricular - prevention & control Male Membrane Potentials Monocrotaline Myocytes, Cardiac - drug effects Myocytes, Cardiac - metabolism Myocytes, Cardiac - pathology Myosin Heavy Chains - metabolism Piperazines - pharmacology Pulmonary Artery - drug effects Pulmonary Artery - metabolism Pulmonary Artery - physiopathology Ranolazine Rats Rats, Sprague-Dawley Sodium - metabolism Sodium Channel Blockers - pharmacology Sodium Channels - drug effects Sodium Channels - metabolism Time Factors Vascular Remodeling - drug effects Vascular Resistance - drug effects Ventricular Function, Right - drug effects Ventricular Remodeling - drug effects
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