Aim The aim of this study was to investigate the effect of bosentan (25, 50, 100 mg/kg) on left ventricular contractile function, cardiac fibrosis, and oxidative stress in pressure overload-induced cardiac hypertrophy in rats.Methods Male rats (200-250 g) were assigned into various groups, namely, sham, aortic constriction, aortic constriction + bosentan (25, 50, and 100 mg/kg), and sham + bosentan (100 mg/kg). Myocardial hypertrophy was produced by constriction of the abdominal aorta. Four weeks after treatment with bosentan (25, 50, and 100 mg/kg perorally), the left ventricular contractile function was measured using a Millar catheter and ECG was carried out.Results Treatment with bosentan (50 and 100 mg/kg perorally) significantly and dose-dependently (P < 0.01 and <0.001) restored hemodynamic parameters including ECG, blood pressure, and left ventricular function. It also significantly elevated the levels of biochemical markers (P < 0.001), that is, superoxide dismutase, reduced glutathione, and membrane-bound inorganic phosphate enzymes like Na + -K + -ATPase and Ca 2 + -ATPase. The elevated levels of creatine kinase-MB and lactate dehydrogenase enzymes, as well as the activities of malondialdehyde and tumor necrosis factor-a, were significantly attenuated (P < 0.05 and <0.001) by bosentan (50 and 100 mg/kg perorally) treatment. An upregulation in the mRNA expression of endothelin-1 was significantly (P < 0.05 and <0.001) attenuated by bosentan (50 and 100 mg/kg perorally) treatment. Histological aberration induced after pressure overload was restored by bosentan treatment.Conclusion Bosentan attenuates the development of cardiac hypertrophy by blocking the endothelin-1 receptor and improving left ventricular function; it also ameliorates endogenous biomarkers in pressure overload-induced cardiac hypertrophy in rats. Cardiovasc