Document Detail


Effect of AT1 receptor blockade on hepatic redox status in SHR: possible relevance for endothelial function?
MedLine Citation:
PMID:  12775556     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The study investigated whether the amelioration of endothelial dysfunction by candesartan (2 mg.kg-1.day-1; 10 wk) 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 + NG-nitro-l-arginine methyl ester (l-NAME) 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 + l-NAME contractions in both strains. Expression of aortic endothelial nitric oxide synthase (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 the hepatic redox system, where ANG II is clearly involved. The results further support the key role of ANG II via AT1 receptors for the functional and structural vascular alterations produced by hypertension.
Authors:
Eva Cediel; David Sanz-Rosa; M Pilar Oubina; Natalia de las Heras; Francisco R González Pacheco; Onofre Vegazo; Javier Jiménez; Victoria Cachofeiro; Vicente Lahera
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2003-05-29
Journal Detail:
Title:  American journal of physiology. Regulatory, integrative and comparative physiology     Volume:  285     ISSN:  0363-6119     ISO Abbreviation:  Am. J. Physiol. Regul. Integr. Comp. Physiol.     Publication Date:  2003 Sep 
Date Detail:
Created Date:  2003-08-11     Completed Date:  2003-09-24     Revised Date:  2013-05-28    
Medline Journal Info:
Nlm Unique ID:  100901230     Medline TA:  Am J Physiol Regul Integr Comp Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  R674-81     Citation Subset:  IM    
Affiliation:
Departamento de Fisiología, Facultad de Medicina, Universidad Complutense, Madrid 28040, Spain.
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MeSH Terms
Descriptor/Qualifier:
Angiotensin II / metabolism
Angiotensin Receptor Antagonists*
Animals
Antihypertensive Agents / pharmacology
Aorta / metabolism,  pathology
Benzimidazoles / pharmacology
Blood Pressure / drug effects,  physiology
Endothelium, Vascular / metabolism*,  pathology
Gene Expression Regulation, Enzymologic / drug effects
Glutathione / metabolism
Glutathione Disulfide / metabolism
Glutathione Peroxidase / metabolism
Glutathione Reductase / metabolism
Hypertension / drug therapy*,  metabolism,  pathology
Liver / drug effects,  metabolism*
Malondialdehyde / metabolism
Membrane Transport Proteins*
NADPH Dehydrogenase / genetics
NADPH Oxidase
Nitric Oxide / metabolism
Nitric Oxide Synthase / genetics
Nitric Oxide Synthase Type III
Oxidation-Reduction
Oxidative Stress / drug effects
Phosphoproteins / genetics
Rats
Rats, Inbred SHR
Rats, Inbred WKY
Receptor, Angiotensin, Type 1
Tetrazoles / pharmacology
Chemical
Reg. No./Substance:
0/Angiotensin Receptor Antagonists; 0/Antihypertensive Agents; 0/Benzimidazoles; 0/Membrane Transport Proteins; 0/Phosphoproteins; 0/Receptor, Angiotensin, Type 1; 0/Tetrazoles; 10102-43-9/Nitric Oxide; 11128-99-7/Angiotensin II; 27025-41-8/Glutathione Disulfide; 542-78-9/Malondialdehyde; 70-18-8/Glutathione; EC 1.11.1.9/Glutathione Peroxidase; EC 1.14.13.39/Nitric Oxide Synthase; EC 1.14.13.39/Nitric Oxide Synthase Type III; EC 1.14.13.39/Nos3 protein, rat; EC 1.6.3.1/CYBA protein, human; EC 1.6.3.1/NADPH Oxidase; EC 1.6.99.1/NADPH Dehydrogenase; EC 1.8.1.7/Glutathione Reductase; S8Q36MD2XX/candesartan

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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