Control of Oxygen Delivery to Renal Tissue by Arterial-to-Venous Oxygen Shunting
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    Control of Oxygen Delivery to Renal Tissue by Arterial-to-Venous Oxygen Shunting

    Regulation of tissue oxygenation within relatively tight limits is a physiological imperative. Tissue hypoxia compromises tissue function and cellular integrity, and in the kidney is a major factor in the pathophysiology of acute and chronic renal failure. Tissue hyperoxia also causes tissue damage through production of reactive oxygen species, although it is not known whether this contributes to kidney disease. Specific mechanisms have evolved to regulate tissue oxygenation through local regulation of blood flow and gene expression. However, in this respect the kidney is unusual since its function, filtration of the plasma and formation of urine, requires that renal blood flow (RBF) greatly exceeds renal metabolic needs. The kidney also regulates systemic oxygenation, through hypoxia inducible factor-dependent production of erythropoietin.

    Thus, we need to understand renal oxygenation both because it is a factor in human disease, and because renal function dictates that the mechanisms regulating oxygenation in the kidney likely differ from those in other organs.

    In this project a combination of experiments and computational models are being used to test the proposal that oxygen levels in the kidney is mediated by arterial-to-venous (AV) O2 shunting.


    2010-2012 NH&MRC 606601 Hypoxia is the common pathway to renal failure, R Evans, J Bertram, M Schlaich, B Gardiner D Smith, J Phillips, $476,000


    Evans, R.G., B.S Gardiner, D.W. Smith, P.M. O'Connor, Intrarenal oxygenation: unique challenges and the biophysical basis of homeostasis. American Journal of Physiology - Renal Physiology 295: F1259F1270, 2008.


    Evans, R.G., B.S Gardiner, D.W. Smith, P.M. O'Connor, Methods for studying the physiology of kidney oxygenation. Clinical and Experimental Pharmacology and Physiology, 35: 14051412, 2008.

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