We examined the mechanisms that maintain stable renal tissue oxygen tension (PO2) during moderate renal ischemia, when changes in renal oxygen delivery (DO2) and consumption (VO2) are mis-matched. When renal artery pressure was reduced progressively from 80 to 40 mmHg, VO2 (-38+/-7 ) was reduced more than DO2 (-26+/-4 ). Electrical stimulation of the renal nerves (RNS) reduced DO2 (-49+/-4 at 2 Hz) more than VO2 (-30+/-7 at 2 Hz). Renal arterial infusion of angiotensin II reduced DO2 (-38+/-3 ) but not VO2 (+10+/-10 ). Despite mis-matched changes in DO2 and VO2, renal tissue PO2 remained remarkably stable when renal artery pressure was 40 mmHg or more, during RNS at 2 Hz or less and during angiotensin II infusion. The ratio of sodium reabsorption and VO2 was reduced by all three ischemic stimuli. None of the stimuli significantly altered the gradients in PCO2 or pH across the kidney. Fractional oxygen extraction increased and renal venous PO2 fell during 2 Hz RNS and angiotensin II infusion, but not when renal artery pressure was reduced to 40 mmHg. Thus, reduced renal VO2 can help prevent tissue hypoxia during mild renal ischemia, but when renal VO2 is reduced less than DO2 other mechanisms prevent a fall in renal PO2. These mechanisms do not include increased efficiency of renal oxygen utilization for sodium reabsorption, or reduced washout of carbon dioxide from the kidney leading to increased oxygen extraction. However, increased oxygen extraction could be driven by altered counter-current exchange of carbon dioxide and/or oxygen between renal arteries veins. Key words: carbon dioxide, hypoxia, oxygen, angiotensin II.