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RENAL PREGLOMERULAR ARTERIAL–VENOUS O 2 SHUNTING IS A STRUCTURAL ANTI‐OXIDANT DEFENCE MECHANISM OF THE RENAL CORTEX
Author(s) -
O’Connor Paul M,
Anderson Warwick P,
Kett Michelle M,
Evans Roger G
Publication year - 2006
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.2006.04391.x
Subject(s) - shunting , kidney , renal cortex , peritubular capillaries , microcirculation , hypoxia (environmental) , renal blood flow , medicine , renal function , venous blood , chemistry , oxygen , organic chemistry
SUMMARY1 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 P o 2 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 P o 2 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 P o 2 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.