Tissue oxygen levels are tightly regulated in all organs. This poses a challenge for the kidney, as its function requires blood flow, and so oxygen delivery, to greatly exceed its metabolic requirements. Because superoxide production in the kidney is dependent on oxygen availability, tissue hyperoxia could drive oxidative stress. In the mammalian renal cortex, this problem may have been solved in part through a structural antioxidant defence mechanism. That is, arteries and veins are closely associated in a counter-current arrangement, facilitating diffusional arterial-to-venous (AV) oxygen shunting. Because of this mechanism, a proportion of the oxygen delivered in the renal artery never reaches kidney tissue, but instead diffuses to the closely associated renal veins, so limiting oxygen transport to tissue. In the non-mammalian kidney arteries and veins are not arranged in an intimate counter-current fashion as in mammals, so AV oxygen shunting is likely less important in regulation of kidney oxygenation in these species. Instead, the kidney s blood supply is predominately of venous origin. This likely has a similar impact on tissue oxygenation as AV oxygen shunting, of limiting delivery of oxygen to renal tissue. Thus, we hypothesise the evolution of structural antioxidant mechanisms that are anatomically divergent, but functionally homologous, in the mammalian and non-mammalian kidney.
|Pages (from-to)||R723 - R727|
|Number of pages||5|
|Journal||American Journal of Physiology - Regulatory Integrative and Comparative Physiology|
|Publication status||Published - 2010|