Renal preglomerular arterial-venous O2 shunting is a structural anti-oxidant defence mechanism of the renal cortex

1. High blood flow to the kidney facilitates a high glomerular filtration rate, but total renal O-2 delivery greatly exceeds renal metabolic requirements. However, tissue PO2 in much of the renal cortex is lower than may be expected, being similar to that of other organs in which perfusion is closely matched to metabolic demand. 2. The lower than expected renal cortical PO2 is now attributed largely to diffusional shunting of as much as 50% of inflowing O-2 from blood within preglomerular arterial vessels to post-glomerular venous vessels. However, the functional significance of this O-2 shunting remains unclear. Indeed, this mechanism may appear maladaptive, given the kidney's susceptibility to hypoxic insults. 3. We hypothesize that renal preglomerular arterial-venous O-2 shunting acts to protect the kidney from the potentially damaging consequences of tissue hyperoxia. The diffusion of O-2 from arteries to veins within the kidney acts to reduce the O-2 content of the blood before it is distributed to the renal microcirculation. Because high tissue PO2 may increase the production of reactive oxygen species, we suggest that renal arterial-venous O-2 shunting may provide a physiological benefit to the organism by limiting O-2 delivery to renal tissue, thereby reducing the risk of cellular oxidation.