Feedforward sympathetic coronary vasodilation in exercising dogs

Department of Physiology and Biophysics,University of Washington School of Medicine, Seattle, Washington 98195-7290 The hypothesis that exercise-induced coronary vasodilation is a result of sympathetic activation of coronary smooth muscle -adrenoceptors was tested. Ten dogs were chronically instrumented with a flow transducer on the circumflex coronary artery and catheters in the aorta and coronary sinus. During treadmill exercise, coronary venous oxygen tension decreased with increasing myocardial oxygen consumption, indicating an imperfect match between myocardial blood flow and oxygen consumption. This match was improved after -adrenoceptor blockade with phentolamine but was significantly worse than control after + -adrenoceptor blockade with phentolamine plus propranolol. The response after -adrenoceptor blockade included local metabolic vasodilation plus a -adrenoceptor vasodilator component, whereas the response after + -adrenoceptor blockade contained only the local metabolic vasodilator component. The large difference in coronary venous oxygen tensions during exercise between -adrenoceptor blockade and + -adrenoceptor blockade indicates that there is significant feedforward -adrenoceptor coronary vasodilation in exercising dogs. Coronary venous and estimated myocardial interstitial adenosine concentrations did not increase during exercise before or after + -adrenoceptor blockade, indicating that adenosine levels did not increase to compensate for the loss of feedforward -adrenoceptor-mediated coronary vasodilation. These results indicate a meaningful role for feedforward -receptor-mediated sympathetic coronary vasodilation during exercise. coronary blood flow; norepinephrine; adenosine; feedback control