Left circumflex coronary blood flow (CBF) was measured in eight mongrel dogs with 8 MHz continuous wave Doppler flow transducers during classical aversive conditioning. The cardiovas-cular condition response consisted of significant (P < 0.01) increases in: (1) mean aortic pressure (16.1%), (2) d(left ventricular pressure)/dt (64.2%), and (3) heart rate (63.2%). The coronary vascular response to behavioral stress consisted of an initial late diastolic decrease in CBF (12.5%) between 5 and 10 seconds after conditional stimulus onset, followed by a significant increase in CBF (96.8%). Concurrently, late diastolic coronary vascular resistance (CVR) first significantly increased (21.9%), then significantly decreased (39.8%). The increase in CVR was attenuated by cardiac pacing and converted into a significant decrease after a-receptor blockade. The decrease in CVR was reduced either by cardiac pacing or cardioselective ^-receptor blockade and eliminated by the combination of a-and /J-receptor blockade. Thus, these data indicate that the coronary vascular response to stress consisted of two components: an initial o-adrenergic coronary vasoconstriction, followed by a more complex vasodilation which was probably mediated by metabolites released secondarily to increases in heart rate and inotropic state. Circ Res 48: 214-223, 1981 WHEN an organism faces an unpleasant or life-threatening situation, a variety of circulatory adjustments must be made to either fight or flee the danger. Important adaptations must occur at the heart, particularly the coronary vessels, so that the increased nutritive demands of the organism can be matched immediately without impairing cardiac function. Thus the survival benefits of a rapidly responding coronary vascular system cannot be un-derstated. Yet, in spite of the importance of this response system, very little information is available on the mechanism(s) mediating the coronary vas-cular response to emotional stress. Excitatory stimuli have been demonstrated to produce intense activation of the sympathetic nervous system (Cohen and Obrist, 1975). Sympathetic stimulation of the myocardium indirectly affects coronary vessel diameter by increases in the chron-otropic and inotropic state of the heart. These, in turn, increase myocardial oxygen consumption and thereby increase coronary blood flow (CBF), presumably through the release of vasodilatory me-tabolites (Rubio and Berne, 1975). The task of characterizing the direct sympathetic control of coronary vascular diameter is complicated since coronary smooth muscle contains both a-and yS-adre