Pulmonary arterial hypertension (PAH) is a common pathophysiologic syndrome defined by a progressive increase in pulmonary vascular resistance and pulmonary artery pressure, eventually leading to right ventricular failure and premature death. Despite recent progress in treating PAH, successful disease management has yet to be accomplished. The rennin angiotensin system has been previously implicated in the pathogenesis of PAH. Using a monocrotaline-induced rat model of PAH, we report that telmisartan, an angiotensin II type 1 receptor blocker, effectively ameliorates pulmonary hypertension, right ventricular hypertrophy and pulmonary vascular inflammation. At the molecular level, we show that telmisartan modulates the levels of angiotensin-converting enzyme 2 (ACE2) in pulmonary arterioles and attenuates monocrotaline-induced increases in the expression of matrix metalloproteinase (MMP)-2 and MMP-9, enzymes critical for vascular remodeling. Our results suggest that telmisartan is a promising therapeutic candidate for PAH and its mechanism of action likely involves upregulating ACE2 and suppressing MMP-mediated vascular remodeling.