Volume overload-induced cardiac hypertrophy is characterized by normal coronary reserve and maximal flow. Accordingly, we tested the hypothesis that both arteriolar and capillary growth are proportional to the magnitude of hypertrophy in this model. Five months after performing an aortocaval fistula [arteriovenous (A-V) shunt] in young rats, right and left ventricles were 61 and 55%, respectively, heavier than their sham controls. Using morphometric methods and image analysis, we found that increases in cardiac myocyte cross-sectional area accounted for approximately 50% of the hypertrophy and that arteriolar length density (LV) (7.5 +/- 0.9 and 7.0 +/- 0.4 mm/mm3) and the frequency distribution of arteriolar diameters were similar in the hearts from A-V shunt and control rats. Capillary LV in the right ventricle was similar in the two groups; in the left ventricle a significantly lower LV for the A-V shunt rats was noted only in the endomyocardium. Capillary volume density was not attenuated in the A-V shunt rats, since slightly larger luminal diameters compensated for any decrements in LV in the left ventricle. These findings provide an anatomic basis for the observation that maximal myocardial perfusion is not necessarily compromised in ventricular enlargement due to aortocaval fistula. Because diastolic volume is increased in this model and thereby provides a stretch on the microvasculature, our findings are consistent with those from other models of cardiac hypertrophy in which enhancement of mechanical factors is associated with angiogenesis.