Renal oxygen delivery: Matching delivery to metabolic demand

The kidneys are second only to the heart in terms of O-2 consumption; however, relative to other organs, the kidneys receive a very high blood flow and oxygen extraction in the healthy kidney is low. Despite low arterial-venous O-2 extraction, the kidneys are particularly susceptible to hypoxic injury and much interest surrounds the role of renal hypoxia in the development and progression of both acute and chronic renal disease. Numerous regulatory mechanisms have been identified that act to maintain renal parenchymal oxygenation within homeostatic limits in the in vivo kidney. However, the processes by which many of these mechanisms act to modulate renal oxygenation and the factors that influence these processes remain poorly understood. A number of such mechanisms specific to the kidney are reviewed herein, including the relationship between renal blood flow and O-2 consumption, pre- and post-glomerular arterial-venous O-2 shunting, tubulovascular cross-talk, the differential control of regional kidney blood flow and the tubuloglomerular feedback mechanism. The roles of these mechanisms in the control of renal oxygenation, as well as how dysfunction of these mechanisms may lead to renal hypoxia, are discussed.