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Journal of Biomedicine and Biotechnology
Volume 2011 (2011), Article ID 469481, 8 pages
Research Article

Effects of Clofibrate on Salt Loading-Induced Hypertension in Rats

1Departamento de Fisiología, Facultad de Medicina, 18012 Granada, Spain
2Hospital Universitario Virgen de las Nieves, Unidad Experimental, 18014 Granada, Spain
3UGC-Olula del Río, 4860 Almeria, Spain
4Departamento de Ciencias de la Salud, Universidad de Jaén, 23071 Jaén, Spain

Received 21 June 2010; Accepted 2 October 2010

Academic Editor: Andrea Vecchione

Copyright © 2011 Antonio Cruz 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.


The effects of clofibrate on the hemodynamic and renal manifestations of increased saline intake were analyzed. Four groups of male Wistar rats were treated for five weeks: control, clofibrate (240 mg/kg/day), salt (2% via drinking water), and s a l t + c l o b r a t e . Body weight, systolic blood pressure (SBP), and heart rate (HR) were recorded weekly. Finally, SBP, HR, and morphologic, metabolic, plasma, and renal variables were measured. Salt increased SBP, HR, urinary isoprostanes, NOx, ET, vasopressin and proteinuria and reduced plasma free T 4 ( F T 4 ) and tissue F T 4 and F T 3 versus control rats. Clofibrate prevented the increase in SBP produced by salt administration, reduced the sodium balance, and further reduced plasma and tissue thyroid hormone levels. However, clofibrate did not modify the relative cardiac mass, NOx, urinary ET, and vasopressin of saline-loaded rats. In conclusion, chronic clofibrate administration prevented the blood pressure elevation of salt-loaded rats by decreasing sodium balance and reducing thyroid hormone levels.