The impact of experimentally induced cardiac hypertrophy on cardiac haemodynamic parameters and inotropic responses is not fully understood. This study aimed to quantify the durational effect of thyroxine(T4)-induced cardiac hypertrophy on the haemodynamic and cardiac function parameters and to investigate how they responded when challenged with the β-adrenoceptor agonist, isoprenaline, before and following blockade of nitric oxide (NO) production with the NO synthase inhibitor NG-nitro-L-arginine (L-NAME). Heart hypertrophy was induced by 7- and 14-day regimes of intra-peritoneal T4 treatment. Eight controls, nine T4-7 and nine T4-14 cardiac hypertrophied male Wistar rats (250-290g), respectively, were anaesthetized i.p. with 1.0 ml chloralose/urethane mixture (16.5/250 mg/ml, respectively) and prepared for in vivo measurement of haemodynamic and cardiac function parameters. Heart weights were higher in the group given T4 for both 7 days and 14 days than control group 14% and 19% (P<0.05), respectively. This was associated with an increase in heart rate, maximum dP/dt and contractility index by 16%, 34% and 14% (P<0.05) respectively in the T4-14 rats. The L-NAME increased the basal levels of blood pressure, heart rate, contractility index and maximum dP/dt by 39%, 23%, 32% and 27% (P<0.05) respectively in T4-14 rats. The L-NAME also augmented the isoprenaline’s inotropic effect in both T4-7 and T4-14 hypertrophied hearts but had no effect on basal myocyte contractility. The T4-14 heart hypertrophy rats showed reduced stress endurance capacity compared to both control and 7 days heart hypertrophy rats. The haemodynamic and cardiac function parameters were significantly enhanced after 14 days thyroxine-induced cardiac hypertrophy indicating increased cardiac performance1. Furthermore, the L-NAME caused significant augmentation of the isoprenaline inotropic effect, in addition to the enhanced effect on the basal cardiac performance in the 14 days hypertrophy hearts. A more severe degree of cardiac hypertrophy was associated with a reduction in stress endurance capacity.