Beta1-adrenoceptor antagonist, metoprolol attenuates cardiac myocyte Ca²⁺ handling dysfunction in rats with pulmonary artery hypertension.

ABSTRACT: Right heart failure is the major cause of death in Pulmonary Artery Hypertension (PAH) patients but is not a current, specific therapeutic target. Pre-clinical studies have shown that adrenoceptor blockade can improve cardiac function but the mechanisms of action within right ventricular (RV) myocytes are unknown. We tested whether the β₁-adrenoceptor blocker metoprolol could improve RV myocyte function in an animal model of PAH, by attenuating adverse excitation-contraction coupling remodeling. PAH with RV failure was induced in rats by monocrotaline injection. When PAH was established, animals were given 10 mg/kg/day metoprolol (MCT + BB) or vehicle (MCT). The median time to the onset of heart failure signs was delayed from 23 days (MCT), to 31 days (MCT + BB). At 23 ± 1 days

SUBMITTER: Fowler ED 

PROVIDER: S-EPMC6013283 | biostudies-literature | 2018 Jul

REPOSITORIES: biostudies-literature