Contribution of serotonin to cardiac remodeling associated with hypertensive diastolic ventricular dysfunction in rats.

Date publication

novembre 2015

Journal

Journal of hypertension

Auteurs

Membres identifiés du Cancéropôle Est :
Pr MONASSIER Laurent

Tous les auteurs :
Ayme-Dietrich E, Marzak H, Lawson R, Mokni W, Wendling O, Combe R, Becker J, El Fertak L, Champy MF, Matz R, Andriantsitohaina R, Doly S, Boutourlinsky K, Maroteaux L, Monassier L

Lien Pubmed

https://www.ncbi.nlm.nih.gov/pubmed/26259125

Résumé

Left-ventricular hypertrophy and interstitial fibrosis are the main pathophysiological factors of heart failure with preserved ejection fraction. Blockade of the serotonin 5-HT2B receptor (5-HT2BR) has been shown to reduce cardiac hypertrophy, oxidative stress, and extracellular cell matrix activation. In this study, we evaluated the effects of the 5-HT2BR blockade, on hemodynamic and cardiac remodeling, in spontaneously hypertensive rats (SHRs) that display a diastolic dysfunction with preserved ejection fraction.

Mots clés

Animals, Blood Pressure, drug effects, Echocardiography, Heart Failure, metabolism, Heart Ventricles, drug effects, Hypertension, metabolism, Hypertrophy, Left Ventricular, metabolism, Male, Mice, Mice, Knockout, Natriuretic Peptide, Brain, metabolism, Pyrimidines, pharmacology, Rats, Rats, Inbred SHR, Receptor, Serotonin, 5-HT2A, genetics, Receptor, Serotonin, 5-HT2B, genetics, Serotonin, metabolism, Serotonin Antagonists, pharmacology, Ventricular Dysfunction, Left, metabolism

Référence

J Hypertens. 2015 11;33(11):2310-21