Previous studies of intra-renal perfusion and tissue oxygenation have produced a wide range of results and have not matched tissue oxygen tension (PtO₂) with concurrent changes in flow in three distinct regions. We thus used an anesthetized rat model of hemorrhage-reperfusion to address this question. Combined PtO₂/laser Doppler fiber-optic probes were simultaneously sited in cortical, corticomedullary (CMJ) and medullary regions of the left kidney. Total renal blood flow was measured in separate experiments. Recordings were made during exsanguination of 10% and 20% of estimated blood volume at 10 minute intervals, followed by shed-blood resuscitation after a further 10 minutes. The decay in PtO₂ was then recorded following total cessation of blood flow, allowing estimation of local oxygen consumption. During exsanguination the PtO2 was maintained in all intra-renal regions, despite significant falls in blood pressure and total renal blood flow. However, intra-renal flow was re-distributed with reduced cortical, unchanged CMJ and increased medullary blood flow. After resuscitation, significant rises above baseline were seen in BP and in PtO₂ across all regions. Whereas cortical and medullary flows regained baseline values, CMJ flow fell. The ratio of PtO₂ to microvascular blood flow increased significantly in all regions during resuscitation, suggesting decreased oxygen consumption. On total cessation of blood flow, the cortex and CMJ showed significant increases in the oxygen decay half-life, consistent with decreased consumption. To our knowledge, this is the first quantitative demonstration of a markedly heterogeneous intra-renal cardiorespiratory response to a hemodynamic insult, with effects most marked at the cortico-medullary junction.