Abstract
When red blood cells reach a low oxygen environment they release a small amount of ATP into the plasma. The ATP and its breakdown products ADP and AMP act on capillary endothelial purinergic receptors to initiate a vasodilator response that is conducted upstream. This forms the basis of a local metabolic feedback control mechanism where the red blood cell is the sensor of the balance of oxygen delivery (flow) versus oxygen consumption by the heart. This is a paradigm shift from the previous idea that the myocardium acts as the sensor of oxygen balance. The existence of feed forward control of the coronary circulation by sympathetic beta adrenoceptor vasodilation, and a modest alpha adrenoceptor vasoconstriction adds complexity and redundancy. A mathematical computer model has been developed to understand the simultaneous action of feedback and feed forward control of coronary blood flow. Data from canine experiments during control exercise and with adrenergic and purinergic receptor blockade were analyzed to elucidate the simultaneous interplay between local metabolic feedback control, and feed forward coronary control. The results indicate that ~71% of coronary vasodilation is due to purinergic local metabolic control and ~27% is due to feed forward adrenergic control during exercise.Grant Funding Source: NIH U01 HL 118738
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