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

We examined the mechanisms that maintain stable renal tissue Po ₂ during moderate renal ischemia, when changes in renal oxygen delivery (Ḋo ₂) and consumption (V̇o ₂) are mismatched. When renal artery pressure (RAP) was reduced progressively from 80 to 40 mmHg, V̇o ₂ (-38 ± 7%) was reduced more than Ḋo ₂ (-26 ± 4%). Electrical stimulation of the renal nerves (RNS) reduced Ḋo ₂ (-49 ± 4% at 2 Hz) more than V̇o ₂ (-30 ± 7% at 2 Hz). Renal arterial infusion of angiotensin II reduced Ḋo ₂ (-38 ± 3%) but not V̇o ₂ (+10 ± 10%). Despite mismatched changes in Ḋo ₂ and V̇o ₂, renal tissue Po ₂ remained remarkably stable at ≥40 mmHg RAP, during RNS at ≤2 Hz, and during angiotensin II infusion. The ratio of sodium reabsorption to V̇o ₂ was reduced by all three ischemic stimuli. None of the stimuli significantly altered the gradients in PCO ₂ or pH across the kidney. Fractional oxygen extraction increased and renal venous Po ₂ fell during 2-Hz RNS and angiotensin II infusion, but not when RAP was reduced to 40 mmHg. Thus reduced renal V̇o ₂ can help prevent tissue hypoxia during mild renal ischemia, but when renal V̇o ₂ is reduced less than Ḋo ₂, other mechanisms prevent a fall in renal Po ₂. 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.