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1 Department of Physiology, School of Medicine, Universidad Complutense, Madrid, Spain
2 Department of Nephrology, Fundacion Jimenez Diaz, Madrid, Spain
3 Medical Department AstraZeneca Farmaceutica, Spain
* To whom correspondence should be addressed. E-mail: vlahera{at}med.ucm.es.
The study investigated whether the amelioration of endothelial dysfunction by candesartan (2 mg/Kg/d; 10 weeks) in spontaneously hypertensive rats (SHR) was associated with modification of hepatic redox system. Systolic arterial pressure (SAP) was higher (p<0.05) in SHR than in Wistar Kyoto rats (WKY) and was reduced (p<0.05) by candesartan in both strains. Acetylcholine (Ach) relaxations were smaller (p<0.05) and contractions induced by Ach+LNAME were greater (p<0.05) in SHR than in WKY. Treatment with candesartan enhanced (p<0.05) Ach-relaxations in SHR and reduced (p<0.05) Ach+LNAME contractions in both strains. Expression of aortic eNOS mRNA was similar in WKY and SHR, and candesartan increased (p<0.05) it in both strains. Aortic mRNA expression of the subunit p22phox of NAD(P)H oxidase was higher (p<0.05) in SHR than in WKY. Treatment with candesartan reduced (p<0.05) p22phox expression only in SHR. Malonyl dialdehyde (MDA) levels were higher (p<0.05) and the ratio reduced/oxidized glutathione (GSH/GSSG) as well as glutathione peroxidase activity (GPx) were lower (p<0.05) in liver homogenates from SHR than from WKY. Candesartan reduced (p<0.05) MDA and increased (p<0.05) GSH/GSSG ratio without affecting GPx. Vessel, lumen and media areas were bigger (p<0.05) in SHR than in WKY. Candesartan treatment reduced (p<0.05) media area in SHR without affecting vessel or lumen area. The results suggest that hypertension is not only associated with elevation of vascular superoxide anions, but with alterations of hepatic redox system, where angiotensin II (A II) is clearly involved. The results further support the key role of A II via AT1 receptors for the functional and structural vascular alterations produced by hypertension.
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