1. Oxygen tension (PO2) in renal cortical tissue can remain relatively constant when renal blood flow changes in the physiological range, even when changes in renal oxygen delivery (DO2) and oxygen consumption (VO2) are mismatched. In the current study, we examined whether this also occurs in the renal medulla and skeletal muscle, or if it is an unusual property of the renal cortex. We also examined the potential for dysfunction of the mechanisms underlying this phenomenon to contribute to kidney hypoxia in disease states associated with increased renal VO2.
2. In both the kidney and hindlimb of pentobarbitone anaesthetized rabbits, whole organ blood flow was reduced by intra-arterial infusion of angiotensin-II and increased by acetylcholine infusion. In the kidney, this was carried out before and during renal arterial infusion of the mitochondrial uncoupler, 2,4-dinitrophenol (DNP), or its vehicle.
3. Angiotensin-II reduced renal (−34%) and hindlimb (−25%) DO2, whereas acetylcholine increased renal (+38%) and hindlimb (+66%) DO2. However, neither renal nor hindlimb VO2 were altered. Tissue PO2 varied with local perfusion in the renal medulla and biceps femoris, but not the renal cortex. DNP increased renal VO2 (+38%) and reduced cortical tissue PO2 (−44%), but both still remained stable during subsequent infusion of angiotensin-II and acetylcholine.
4. We conclude that maintenance of tissue PO2 in the face of mismatched changes in local perfusion and VO2 is an unusual property of the renal cortex. The underlying mechanisms remain unknown, but our current findings suggest they are not compromised when resting renal VO2 is increased.