• Paul M O'Connor, Michelle M Kett, Warwick P Anderson, and Roger G Evans.
• Dept. of Physiology, Medical College of Wisconsin, 8071 Watertown Plank Road, Milwaukee, WI 53266, USA. POconnor@mail.phys.mcw.edu
• Am. J. Physiol. Renal Physiol. 2006 Mar 1;290(3):F688-94.

AbstractThe 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 [Phe(2),Ile(3),Orn(8)]-vasopressin selectively reduced medullary perfusion and Po(2) (-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 4 Hz), cortical perfusion (-57 +/- 17%), and cortical Po(2) (-44 +/- 12%). Medullary tissue Po(2) was reduced by -70 +/- 5% at 4 Hz, 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 ANG II (0.5-5 microg. kg(-1).min(-1)) dose dependently reduced cortical perfusion (up to -65 +/- 3%; P < 0.001) and cortical Po(2) (up to -57 +/- 4%; P < 0.05). However, medullary perfusion was only significantly reduced at the highest dose (5 microg. kg(-1).min(-1); by 29 +/- 6%). Medullary perfusion was not reduced by 1 microg. kg(-1).min(-1) ANG II, but medullary Po(2) 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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