Multiple mechanisms act to maintain kidney oxygenation during renal ischemia in anesthetized rabbits

We examined the mechanisms that maintain stable renal tissue Po2 during moderate renal ischemia, when changes in renal oxygen delivery (Ḋo2) and consumption (V̇o2) are mismatched. When renal artery pressure (RAP) was reduced progressively from 80 to 40 mmHg, V̇o2 (−38 ± 7%) was reduced more than Ḋo2 (−26 ± 4%). Electrical stimulation of the renal nerves (RNS) reduced Ḋo2 (−49 ± 4% at 2 Hz) more than V̇o2 (−30 ± 7% at 2 Hz). Renal arterial infusion of angiotensin II reduced Ḋo2 (−38 ± 3%) but not V̇o2 (+10 ± 10%). Despite mismatched changes in Ḋo2 and V̇o2, renal tissue Po2 remained remarkably stable at ≥40 mmHg RAP, during RNS at ≤2 Hz, and during angiotensin II infusion. The ratio of sodium reabsorption to V̇o2 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 RAP was reduced to 40 mmHg. Thus reduced renal V̇o2 can help prevent tissue hypoxia during mild renal ischemia, but when renal V̇o2 is reduced less than Ḋo2, 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 countercurrent exchange of carbon dioxide and/or oxygen between renal arteries and veins.