The aim of the present study was to evaluate specifically left ventricular (LV) function in rat hearts as they transition from normal to hypertrophic state and back to normal. Either isoproterenol (1.2 and 2.4 mg^.kg^-1. day^-1 for 3 days, Iso group) or vehicle (saline 24 µl^.day^-1 for 3 days, Sa group) was infused by subcutaneous implantation of osmotic minipump. After verifying the development of cardiac hypertrophy, we recorded continuous LV pressure-volume (P-V) loops of in situ ejecting hypertrophied rat hearts. Curved LV end-systolic P-V relation (ESPVR) and systolic P-V area (PVA) were obtained from a series of LV P-V loops in Sa and Iso groups 1 hr or 2 days after removal of osmotic minipump. PVA atmidrange LV volume (PVA_mLVV) was taken as a good index for LV work capability (13,15,20,21). However, in rat hearts during remodeling whether PVA_mLVV is a good index for LV work capability has not been determined yet. In the present study, in contrast to unchanged ESP_mLVV, PVA_mLVV was significantly decreased by isoproterenol treatment relative to saline, however these measurements were the same two days after pump removal. Simultaneous treatment with a ₁-blocker, metoprolol (24 mg^.kg^-1.day^-1) blocked the formation of cardiac hypertrophy and thus PVA_mLVV did not decrease. The reversible changes in PVA_mLVV reflect precisely the changes in LV work capability in isoproterenol-induced hypertrophied rat hearts mediated by ₁-receptor. These results indicate that the present approach may be an appropriate strategy for evaluating the effects of anti-hypertrophic and anti-fibrotic modalities