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Endothelial dysfunction in acute renal failure

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Abstract

The normal vascular endothelium provides an uninterrupted inner lining to the vessel walls, allowing blood to circulate to various parts of the body. Besides providing a conduit for the circulation of blood, the vascular endothelium has now been recognized as possessing several other functions, and is regarded as an active metabolic and endocrine organ [1, 2]. The endothelium selectively “filters” substances, controls hemostasis, interacts with cellular and noncellular components of circulating blood, plays a role in white cell trafficking, synthesizes angiotensin-converting enzyme (ACE), and modulates vasoactive agents such as catecholamines, bradykinin, and angiotensin II [3]. The endothelium also regulates vascular tone directly, through the production and release of both vasodilatory (eg. endothelium derived relaxing factor-nitric oxide, NO, prostacyclin, PGI2) and vasoconstrictive substances (eg. endothelin-1, ET-1) (Table 1). In the kidney, endothelial cells line the intricate intrarenal vasculature, and also contribute as a significant initial layer of the filtration barrier to the passage of blood constituents into the urinary space. With such major functions attributable to the endothelium, perturbations of normal endothelial function lead to a multitude of derangements, including significant hemodynamic alterations in different organ systems in general, and the kidney in particular.

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Agarwal, A., Raij, L. (1998). Endothelial dysfunction in acute renal failure. In: Critical Care Nephrology. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-5482-6_43

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