To attempt to explain the loss of subendocardial coronary reserve in chronic pressure-overload cardiac hypertrophy on a morphologic basis, we measured capillary capacity and coronary artery and arteriole medial wall area in dogs with moderately severe chronic (1 year) left ventricular hypertrophy (LVH). Aortic bands were placed on the ascending aorta of 8-10-week-old puppies of either sex, and hearts were perfusion fixed with 2% glutaraldehyde 8-16 months later after hemodynamic study while fully conscious. Left ventricular (LV) mass/body weight ratio in 11 banded dogs with LV end-diastolic pressure < 12 mmHg was 72% greater than in 15 controls (C). There was a decrease in subendocardial coronary reserve during adenosine-induced vasodilation with a shift away from the subendocardium (endo/epi flow ratio: C = 0.68 +/- 0.05; LVH = 0.34 +/- 0.06; P < 0.05). In spite of the extensive hypertrophy, image analysis revealed capillary density to be equally reduced by only 10-15% in endo, mid and epicardial LV regions compared to control dogs, while increased capillary cross-sectional area resulted in no change in capillary surface area/myocyte volume or volume percentage capillary space. In addition to these data suggesting capillary angiogenesis, there was no reduction in arteriolar density, indicating transmural increase in arteriolar number, and, as a consequence, increased total length of the resistance vessels. Medial area of arterioles and arteries showed a graduated increase according to size. We concluded that due to the lack of transmural difference in vascular morphology in chronic (1 year) moderately severe LVH, these anatomic bases do not play a major role as a cause for the loss of coronary reserve. Regional functional differences as a consequence of the morphologic alterations, however, cannot be excluded.