Quantitative analysis of feedforward sympathetic coronary vasodilation in exercising dogs

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Abstract
Recent experiments demonstrate that feedforward sympathetic β-adrenoceptor coronary vasodilation occurs during exercise. The present study quantitatively examined the contributions of epinephrine and norepinephrine to exercise coronary hyperemia and tested the hypothesis that circulating epinephrine causes feedforward β-receptor-mediated coronary dilation. Dogs (n = 10) were chronically instrumented with a circumflex coronary artery flow transducer and catheters in the aorta and coronary sinus. During strenuous treadmill exercise, myocardial oxygen consumption increased by ∼3.9-fold, coronary blood flow increased by ∼3.6-fold, and arterial plasma epinephrine concentration increased by ∼2.4-fold over resting levels. At arterial concentrations matching those during strenuous exercise, epinephrine infused at rest (n = 6) produced modest increases (18%) in flow and myocardial oxygen consumption but no evidence of direct β-adrenoceptor-mediated coronary vasodilation. Arterial norepinephrine concentration increased by ∼5.4-fold during exercise, and coronary venous norepinephrine was always higher than arterial, indicating norepinephrine release from cardiac sympathetic nerves. With the use of a mathematical model of cardiac capillary norepinephrine transport, these norepinephrine concentrations predict an average interstitial norepinephrine concentration of ∼12 nM during strenuous exercise. Published dose-response data indicate that this norepinephrine concentration increases isolated coronary arteriolar conductance by ∼67%, which can account for ∼25% of the increase in flow observed during exercise. It is concluded that a significant portion of coronary exercise hyperemia (∼25%) can be accounted for by direct feedforward β-adrenoceptor coronary vascular effects of norepinephrine, with little effect from circulating epinephrine.

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