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 V̇o ₂ 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.