An inadequate vascular growth during pressure-overload cardiac hypertrophy involves both pre-capillary and capillary vessels. With the development of hypertrophy in spontaneously hypertensive rats (SHR) coronary reserve declines as indicated by increases in minimal coronary vascular resistance (MCVR). Capillary numerical density, surface density, and volume density also decline. However, after hypertrophy becomes stabilized late in life these parameters return to normal. That elevated blood pressure plays a major role in the decrement in coronary reserve was demonstrated by treating prehypertensive SHR with hydralazine which prevented hypertension but not cardiac hypertrophy. In these animals capillary density remained depressed but coronary reserve was normal. Capillary growth in SHR was, however, stimulated by exercise training even though blood pressure and cardiac hypertrophy were unaffected. Studies on thyroxine-induced cardiac hypertrophy provided evidence of a substantial angiogenesis. In this model coronary reserve is normal or slightly elevated, while capillary density is increased. These studies suggest that angiogenesis is effected by the stimulus evoking cardiac enlargement and that a variety of factors may influence the growth of precapillary and capillary coronary vessels.