The renal medulla works normally on the brink of anoxia. Regulation of oxygen supply and demand in this region is delicately regulated by multiple homeostatic systems (Fig 1). Oxygen demand is reflected by the rate of tubular reabsorption, which is determined by the glomerular filtration rate, delivery of urine to the thick limbs, and control of solute transport by local mediators (Biez|s.§nd.,.Rose.n 1995). Non-steroidal anti-inflammatory drugs inhibit prostaglandin synthesis, precipitating a decline in medullary blood flow and oxygenation. Adenosine, a by-product of ATP released during tissue hypoxia, may augment tubuloglomerular feedback and induce cortical vasoconstriction (reducing glomerular filtration rate) with medullary vasodilatation and tubular transport inhibition to limit medullary hypoxia ( Brezisand Rosen..1995). Similarly, nitric oxide and endothelin induce medullary vasodilatation, and endothelin also causes cortical vasoconstriction. All these vasoactive mediators appear to be co-ordinated to preserve medullary oxygen balance in renal hypoperfusion. Deficient or excessive stimulation of these renal defensive mechanisms may generate medullary oxygen insufficiency and/or ARF (Fig 1).
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