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1 Department of Physiology, Monash University, Melbourne, Victoria, Australia; Department of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin, USA
2 Department of Physiology, Monash University, Melbourne, Victoria, Australia
* To whom correspondence should be addressed. E-mail: POconnor{at}mail.phys.mcw.edu.
The aim of the current study was to determine whether renal medullary oxygenation is independent of the level of cortical blood flow, by testing responses to stimuli that selectively reduce blood flow in either the cortex or medulla. In anesthetized rabbits, renal arterial infusion of [Phe2,Ile3,Orn8]-vasopressin selectively reduced medullary perfusion and pO2 (-54±24% and -50±10% respectively) but did not significantly affect cortical perfusion or tissue oxygenation. In contrast, stimulation of the renal nerves resulted in renal cortical ischemia with reductions in total renal blood flow (-76±3% at 4Hz), cortical perfusion (-57±17%) and cortical pO2 (-44±12%). Medullary tissue pO2 was reduced by -70±5% at 4Hz, despite medullary perfusion being unaffected and distal tubular sodium reabsorption being reduced (by -83.3±1.2% from baseline). In anesthetized rats, in which renal perfusion pressure was maintained with an aortic constrictor, intravenous infusion of angiotensin II (0.5-5µg kg-1min-1) dose-dependently reduced cortical perfusion (up to -65±3%; P<0.001) and cortical pO2 (up to -57±4%; P<0.05). However, medullary perfusion was only significantly reduced at the highest dose (5µg kg-1min-1; by 29±6%). Medullary perfusion was not reduced by 1µg kg-1min-1 angiotensin II, but medullary pO2 was significantly reduced (-12±4%). Thus, although cortical and medullary blood flow may be independently regulated, medullary oxygenation may be compromised during moderate to severe cortical ischemia even when medullary blood flow is maintained.
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