We characterized hemodynamics and systolic and diastolic right ventricular (RV) function in relation to structural changes in the rat model of monocrotaline (MCT)-induced pulmonary hypertension. Rats were treated with 30 mg/kg (MCT30, n=15) or 80 mg/kg (MCT80, n=16) MCT to induce compensated RV hypertrophy or RV failure, respectively. Saline-treated rats served as control (CONT, n=13). After 4 weeks, a pressure-conductance catheter was introduced into the RV to assess pressure-volume relations. Subsequently, rats were sacrificed, hearts and lungs were rapidly dissected, and RV, left ventricle (LV) and interventricular septum (IVS) were weighed and analyzed histochemically. RV/(LV+IVS) weight ratio was 0.29±0.05 in CONT, 0.35±0.05 in MCT30 and 0.49±0.10 in MCT80 rats (p<0.001 vs. CONT and MCT30) confirming MCT-induced RV hypertrophy. RV ejection fraction was 49±6% in CONT, 40±12% in MCT30 (p<0.05 vs. CONT) and 26±6% in MCT80 rats (p<0.05 vs. CONT and MCT30). In MCT30 rats, cardiac output was maintained, but RV volumes and filling pressures were significantly increased compared to CONT (all p<0.05), indicating RV remodeling. In MCT80 rats, RV systolic pressure, volumes and peak wall stress were further increased, and cardiac output was significantly decreased (all p<0.05). However, RV end-systolic and end-diastolic stiffness were unchanged, consistent with the absence of interstitial fibrosis. MCT-induced pressure-overload was associated with a dose-dependent development of RV hypertrophy. The most pronounced response to MCT was an overload-dependent increase of RV end-systolic and end-diastolic volumes, even under non-failing conditions.