If a coronary vascular network is restricted in its ability to carry more BF when stimulated, the distal cardiac tissue it supplies can become hypoxic immediately. The sheer area that the small resistance vessels cover in the myocardium warrants particular attention as a means to influence minute to minute oxygen exchange and impact BF distribution. This perfusion fine tuning is accomplished primarily through vasodilation of the coronary resistance arterioles, but the mechanism that achieves this effect changes significantly as aging occurs and as comorbidities arise. Not surprisingly, advancing age is associated with the increased generation and presence of reactive oxygen species (ROS) in nearly all tissues. This presentation will reconcile how ROS can be successfully utilized during increased metabolic demand as a substrate to mediate vasoreactivity in the coronary microcirculation in young animal models, and how this signaling changes as “normal” aging progresses, thereby setting a stage for the development of heart failure.