The roles of vasodilator metabolites and/or reduced local intra-arteriolar pressure in producing the reactive hyperemia which follows the sudden release of arterial occlusion were studied. It was found that slight increases of metabolic activity during the period of occlusion increased the reactive hyperemia considerably. Maintenance of intra-arteriolar pressure during arterial occlusion depressed the resultant reactive hyperemia. It was concluded that both factors contribute to the reactive hyperemia. The blood flow “debt” incurred during arterial occlusion was almost invariably “overpaid” during the reactive hyperemia period.