Left ventricular hypertrophy (LVH) is an adaptive structural remodelling consequent to uncontrolled blood pressure. Impaired angiogenesis plays a vital role in transiting LVH into cardiac failure. Catecholamines modulates myocardial function through Beta adrenoceptors and their blockers (β-AR) reduces cardiovascular morbidity and mortality by decelerating the LVH progression. Nonetheless, the effect of β-AR blockers on myocardial vascular bed remains largely obscure. Hence, this study is focussed on analysing the possible outcomes of β-AR blocker on myocardial vascular remodelling using surgically induced LVH mice model. Transverse aortic constricted mice and sham operated mice were administered with metoprolol at a dose of 30 mg.kg .day for 60 days and myocardial VEGF alpha levels, GSH/GSSG ratio, Myocardial protein carbonyl content, Hypertrophy index and global myocardial function, trans-aortic fluid dynamics and expression pattern of angiopoietin-1 and VEGF alpha were assesed. These findings were further confirmed by histochemical analysis for myocardial capillary density, perivascular fibrosis ratio and intimal thickening. Sub- chronic β-AR blockade reduced the oxidative stress, hypertrophic index, intimal thickening and perivascular fibrosis ratio. A marked increase in myocardial VEGF, angiopoietin 1, global myocardial function and myocardial capillary density was also observed. There was a reduction in the LVH and upregulation of myocardial angiogenesis concluding that β-AR blockers prevent adverse vascular remodelling which might underlie its concealed mechanism of action.This article is protected by copyright. All rights reserved.