Pulmonary arterial hypertension is a fatal disease,especially when it causes right heart failure (RHF). However, it is difficult to treat. It has been reported thattrapidil (Tra) can improve the redox balance and cardiacconditions. In this study, we investigated the effect of Tra onRHF induced by monocrotaline (MCT) in rats. Male Wistarrats were treated with MCT or Tra. Treatment lasted 28 days,then rats were euthanized after echocardiography and catheterization. Subsequently, lungs and right ventricular myocardiawere evaluated by hematoxylin and eosin, Masson,and TUNEL staining. Protein expression was detected bywestern blotting. We found remarkably expanded rightventricle end-diastolic volume, decreased partial pressureof oxygen (PaO2), increased partial pressure of carbondioxide (PaCO2), right ventricular systolic pressure, meanpulmonary arterial pressure, lung/body weight, and liver/body weight in the RHF rat group, as well as increases inthe apoptosis rate and the expression of endoplasmic reticulumstress (ERS)-related proteins. However, these changes were significantly inhibited by Tra. Our data suggested thatinhibition of ERS is essential for improving RHF, and thattherapeutic intervention of Tra in RHF rats works by reducingERS.