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BioMed Research International
Volume 2014 (2014), Article ID 936978, 10 pages
http://dx.doi.org/10.1155/2014/936978
Research Article

Renal Overexpression of Atrial Natriuretic Peptide and Hypoxia Inducible Factor-1 as Adaptive Response to a High Salt Diet

1Department of Pathophysiology, School of Pharmacy and Biochemistry, University of Buenos Aires, INFIBIOC-CONICET, Argentina
2Cátedra de Fisiopatología, Facultad de Farmacia y Bioquímica, UBA, Junín 956, Piso 5, 1113 Buenos Aires, Argentina
3Laboratory of Experimental Medicine, Hospital Alemán, Buenos Aires, Argentina
4Department of Pharmacology, School of Pharmacy and Biochemistry, University of Buenos Aires, INFIBIOC-CONICET, Argentina
5Department of Clinical Biochemistry, School of Pharmacy and Biochemistry, University of Buenos Aires, INFIBIOC-CONICET, Argentina

Received 27 April 2013; Revised 31 December 2013; Accepted 6 January 2014; Published 13 February 2014

Academic Editor: Christian Mühlfeld

Copyright © 2014 Silvana Lorena Della Penna et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

In the kidney, a high salt intake favors oxidative stress and hypoxia and causes the development of fibrosis. Both atrial natriuretic peptide (ANP) and hypoxia inducible factor (HIF-1) exert cytoprotective effects. We tested the hypothesis that renal expression of ANP and HIF-1 is involved in a mechanism responding to the oxidative stress produced in the kidneys of rats chronically fed a high sodium diet. Sprague-Dawley rats were fed with a normal salt (0.4% NaCl) (NS) or a high salt (8% NaCl) (HS) diet for 3 weeks, with or without the administration of tempol (T), an inhibitor of oxidative stress, in the drinking water. We measured the mean arterial pressure (MAP), glomerular filtration rate (GFR), and urinary sodium excretion (). We evaluated the expression of ANP, HIF-1, and transforming growth factor (TGF-1) in renal tissues by western blot and immunohistochemistry. The animals fed a high salt diet showed increased MAP and levels and enhanced renal immunostaining of ANP, HIF-1, and TGF-1. The administration of tempol together with the sodium overload increased the natriuresis further and prevented the elevation of blood pressure and the increased expression of ANP, TGF-1, and HIF-1 compared to their control. These findings suggest that HIF-1 and ANP, synthesized by the kidney, are involved in an adaptive mechanism in response to a sodium overload to prevent or attenuate the deleterious effects of the oxidative stress and the hypoxia on the development of fibrosis.