The effect of intracoronary norepinephrine (NE) infusion in a dose of 2 microgram/min on postocclusion hyperaemic reactions following occlusions of 15 sec, 30 sec, 60 sec, and 120 sec was studied on isolated fibrillating, blood-perfused canine hearts. Basal perfusion pressure was kept at the level of 150 mm Hg; perfusion was done with constant pressure or constant volume. During administration of NE, basal flow and basal coronary conductance increased with both perfusion techniques. In the postocclusion period during administration of NE, peak conductance, maximum conductance, reactivity, mean transit time of reactive hyperaemia, postocclusive conductance area and repayment decreased. The differences found in postocclusion reactions in the control state originated from the different perfusion techniques disappeared when NE was infused. The phenomena may be explained by the stimulation of alpha and beta receptors as well as of myocardial metabolism by NE. The results support earlier views which ascribe a decisive role to vasoactive metabolites in the postocclusion reaction after prolonged occlusions. The decrease in reactive hyperaemia by NE may contribute to the development of angina pectoris.