Proposed role of nitric oxide (NO) in radiocontrast-induced acute renal failure (ARF). A, Administration of iothalamate, a radiocon-trast dye, to rats increases medullary blood flow. Inhibitors of either prostaglandin production (such as the NSAID, indomethacin) or inhibitors of NO synthesis (such as L-NAME) abolish the compensatory increase in medullary blood flow that occurs in response to radiocontrast administration. Thus, the stimulation of prostaglandin and NO production after radiocontrast administration is important in maintaining medullary perfusion and oxygenation after administration of contrast agents. B, Radiocontrast stimulates the production of vasodilators (such as prostaglandin [PGy and endothelium-dependent nitric oxide [EDNO]) as well as endothelin and other vasoconstrictors within the normal kidney. The vasodilators counteract the effects of the vasoconstrictors so that intrarenal vasoconstriction in response to radiocontrast is usually modest and is associated with little or no loss of renal function. However, in situations when there is preexisting chronic renal insufficiency (CRF) the vasodilator response to radiocontrast is impaired, whereas production of endothelin and other vasoconstrictors is not affected or even increased. As a result, radiocontrast administration causes profound intrarenal vasoconstriction and can cause ARF in patients with CRF. This hypothesis would explain the predisposition of patients with chronic renal dysfunction, and especially diabetic nephropathy, to contrast-induced ARF. (A, Adapted from Agmon and Brezis [15], with permission; B, from Agmon et al. [16], with permission.)

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