Testosterone and obesity each increase renin‐angiotensin system (RAS) activity. Thus, testosterone may worsen obesity‐related RAS activation, and contribute to cardiovascular dysfunction in obese men. This study determined whether testosterone potentiated effects of obesity on left ventricular (LV) hypertrophy and cardiac fibrosis. Male New Zealand White rabbits were fed a lean or 10% added fat diet. After 12 wks, obese rabbits exhibited increased resting heart rate, systolic blood pressure, plasma renin activity (PRA) and plasma aldosterone. Obese rabbits also exhibited increased LV mass (6.05 ± 0.16 vs. 4.75 ± 0.10 g, respectively, p=0.05) and cardiomyocyte cross‐sectional area (372 ± 19 vs. 305 ± 13 μm2;, respectively; p=0.01) compared to lean rabbits. These hypertrophic effects were attenuated by both castration (5.31 ± 0.26 g; 328 ± 21 μm2) and treatment with the angiotensin type 1 receptor blocker, losartan (5.52 ± 0.23 g; 288 ± 35 μm2). However, castration in obese rabbits did not attenuate obesity‐related increases in PRA or aldosterone. Both castration and losartan in obese rabbits increased matrix metalloproteinase‐2 activity but did not alter tissue inhibitor of matrix metalloproteinase‐1 expression. These results suggest that testosterone contributes to obesity‐related LV hypertrophy and collagen degradation, but does so independently of PRA. Supported by AHA GIA 0655019Y.