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Angiotensin II and endothelin induce inflammation and thereby promote hypertension-induced end-organ damage

Item Type:Article
Title:Angiotensin II and endothelin induce inflammation and thereby promote hypertension-induced end-organ damage
Creators Name:Mueller, D.N. and Fiebeler, A. and Park, J.K. and Dechend, R. and Luft, F.C.
Abstract:Angiotensin (Ang) II and endothelin (ET-1) can both be regulated by NF-{kappa}B. They are, to variable degrees, also capable of activating NF-{kappa}B and increase the expression of NF-{kappa}B-dependent genes. Ang II-related vascular effects are in part mediated by ET-1. Nitric oxide synthase inhibition facilitates Ang II-related effects, which can be inhibited both by AT1-receptor blockers and by endothelin system inhibitors. This state-of-affairs supports the notion that a combined therapeutic strategy of inhibiting Ang II and ET-1 generation or blocking their effects at the receptor level would be superior to either strategy alone. Animal studies are encouraging but not without conflicting results. Angiotensin-converting enzyme inhibitors and AT1-receptor blockers have a superb track record in experimental animal models and in a host of clinical studies. Selective and nonselective blockers of the ET-1 receptors are important research tools and are also undergoing clinical trials. Inhibitors of the endothelin-converting enzyme have been developed. The recent elucidation of the endothelin-converting enzyme's physical structure should facilitate the development of still more novel compounds to inhibit ET-1 generation. We have recently engendered supportive evidence in this regard.
Keywords:Angiotensin II, Endothelin, Inflammation, NF-{kappa}B, End-Organ Demage, Animals
Source:Clinical Nephrology
Page Range:S2-S12
Date:July 2003
PubMed:View item in PubMed

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