Feedforward sympathetic coronary vasodilation in exercising dogs

The hypothesis that exercise-induced coronary vasodilation is a result of s ympathetic activation of coronary smooth muscle beta -adrenoceptors was tes ted. Ten dogs were chronically instrumented with a flow transducer on the c ircumflex coronary artery and catheters in the aorta and coronary sinus. Du ring treadmill exercise, coronary venous oxygen tension decreased with incr easing myocardial oxygen consumption, indicating an imperfect match between myocardial blood flow and oxygen consumption. This match was improved afte r alpha -adrenoceptor blockade with phentolamine but was significantly wors e than control after alpha + beta -adrenoceptor blockade with phentolamine plus propranolol. The response after alpha -adrenoceptor blockade included local metabolic vasodilation plus a beta -adrenoceptor vasodilator componen t, whereas the response after alpha + beta -adrenoceptor blockade contained only the local metabolic vasodilator component. The large difference in co ronary venous oxygen tensions during exercise between alpha -adrenoceptor b lockade and alpha + beta -adrenoceptor blockade indicates that there is sig nificant feedforward beta -adrenoceptor coronary vasodilation in exercising dogs. Coronary venous and estimated myocardial interstitial adenosine conc entrations did not increase during exercise before or after alpha + beta -a drenoceptor blockade, indicating that adenosine levels did not increase to compensate for the loss of feed forward beta -adrenoceptor-mediated coronar y vasodilation. These results indicate a meaningful role for feedforward be ta -receptor-mediated sympathetic coronary vasodilation during exercise.