The aim of the present study was to determine if the relationship between myocardial O2 supply and O2 consumption was preserved after prolonged pressure overload due to aortic valve stenosis. This was examined in anesthetized open-chest dogs in which the aortic valve was plicated 6 months previously. We measured coronary blood flow with radioactive microspheres and regional small vessel O2 saturation with microspectrophotometry, to obtain O2 supply, and O2 consumption. Regional O2 consumption was calculated as the product of flow and O2 extraction. The left ventricular weight/body weight ratio was 81% greater in the dogs with aortic valve stenosis. There were no hemodynamic differences between the groups except that left ventricular systolic pressure was 38 +/- 22 mm Hg greater than aortic in the hypertrophied group. Coronary blood flow did not differ between the control and hypertrophied groups nor were there subepicardial vs subendocardial differences. When maximal coronary flow was determined with chromonar (10 mg/kg), the flow increase was significantly attenuated in the hypertrophied subendocardium (242.1 +/- 82.3 (hypertrophy) vs 512.4 +/- 204.1 ml.min-1.100 g-1 (control). There were no significant differences in O2 extraction or O2 consumption/g between control and hypertrophied animals. There was a significantly lower O2 supply/consumption ratio in the subendocardium compared to the subepicardium of both groups. However, the O2 supply/consumption ratio was not decreased by hypertrophy. Thus, despite significant hypertrophy, a loss of flow reserve and a high left ventricular pressure, O2 supply/consumption balance is preserved in valvular aortic stenosis at rest.