1. Oxygen tension (PO(2) ) in renal cortical tissue can remain relatively constant when renal blood flow changes in the physiological range, even when changes in renal oxygen delivery (DO(2) ) and oxygen consumption (VO(2) ) are mis-matched. In the current study we examined whether this also occurs in the renal medulla and skeletal muscle, or 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 VO(2) . 2. In both the kidney and hind-limb 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 done before and during renal arterial infusion of the mitochondrial uncoupler 2,4-dinitrophenol (DNP) or its vehicle. 3. Angiotensin II reduced renal (-34 ) and hind-limb (-25 ) DO(2) while acetylcholine increased renal (+38 ) and hind-limb (+66 ) DO(2) . However, neither renal nor hind-limb VO(2) were altered. Tissue PO(2) varied with local perfusion in the renal medulla and biceps femoris, but not the renal cortex. DNP increased renal VO(2) (+38 ) and reduced cortical tissue PO(2) (-44 ) but both still remained stable during infusion of angiotensin II and acetylcholine. 4. We conclude that maintenance of tissue PO(2) in the face of mis-matched changes in local perfusion and VO(2) 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 VO(2) is increased.
|Pages (from-to)||247 - 254|
|Number of pages||8|
|Journal||Clinical and Experimental Pharmacology and Physiology|
|Publication status||Published - 2011|