Around 20-35% ofcases dilated cardiomyopathy (DCM) are due to genetic mutations. A mutation incardiac actin— ACTC E361G, has been shown to cause DCM in humans. This mutationhas been stably expressed at around 50% of total actin in a transgenic (TG)mouse-line. Previous work on this TG mouse has shown that the molecularphenotype constitutes an uncoupling of Ca2+-sensitivity from thelevel of troponin I phosphorylation that may cause a blunting of the lusitropicresponse to stress, with consequent heart failure (HF). Despite an absence of awhole animal phenotype under basal conditions, E361G mice show a bluntedresponse to acute dobutamine treatment which would lead to a reduced cardiacreserve. We hypothesise this reduced cardiac reserve may cause the mice todevelop HF when exposed to chronic stress. TG and NTG mice were chronicallyexposed to angiotensin II (1.4mg/kg body weight/day) for 4 weeks using subcutaneouslyimplanted osmotic mini-pumps. Cardiac parameters were measured usingechocardiography prior to implantation (baseline) and weekly throughout the4-week infusion period. By the end of the second week of infusion leftventricular internal dimension was significantly greater in the TG mice (3.71 ± 0.08mm vs 3.48 ± 0.07mm,P=0.0413) thus indicating left ventricular dilation. In conclusion, chroniccardiac stress is necessary to evoke a dilated phenotype in the E361G mouse.