To investigate mechanisms of reactive hyperemia, single arterioles of the hamster cheek pouch were occluded for periods of 1 s-3 min. Arteriolar diameters were measured upstream and downstream from the occlusion. O2 availability to the tissue was controlled by equilibrating the suffusate with low (0% O2) or high (10% O2) O2 gas mixtures. After very brief occlusions downstream sites dilated transiently, but upstream diameters did not change. Upstream and downstream diameters both increased during longer occlusions with O%-O2 and 10%-O2 suffusion. Microvascular pressure decreased at downstream sites and increased at upstream sites within 1-2 s of occlusion. During 0%-O2 suffusion tissue and periarteriolar O2 tensions (PO2's) began to decrease within 2 s of occlusion and had decreased halfway to their minimum value by 7 s. PO2's decreased only slightly during 10%-O2 suffusion. Calculated first-order rate constants for arteriolar diameter recovery decreased and total recovery time increased as occlusion duration was prolonged. This study suggests that multiple mechanisms (metabolic, myogenic, and passive) contribute to reactive hyperemia.