Document Detail


Aldosterone induces a vascular inflammatory phenotype in the rat heart.
MedLine Citation:
PMID:  12384457     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Vascular inflammation was examined as a potential mechanism of aldosterone-mediated myocardial injury in uninephrectomized rats receiving 1% NaCl-0.3% KCl to drink for 1, 2, or 4 wk and 1) vehicle, 2) aldosterone infusion (0.75 microg/h), or 3) aldosterone infusion (0.75 microg/h) plus the selective aldosterone blocker eplerenone (100 mg. kg(-1). day(-1)). Aldosterone induced severe hypertension at 4 wk [systolic blood pressure (SBP), 210 +/- 3 mmHg vs. vehicle, 131 +/- 2 mmHg, P < 0.001], which was partially attenuated by eplerenone (SBP, 180 +/- 7 mmHg; P < 0.001 vs. aldosterone alone and vehicle). No significant increases in myocardial interstitial collagen fraction or hydroxyproline concentration were detected throughout the study. However, histopathological analysis of the heart revealed severe coronary inflammatory lesions, which were characterized by monocyte/macrophage infiltration and resulted in focal ischemic and necrotic changes. The histological evidence of coronary lesions was preceded by and associated with the elevation of cyclooxygenase-2 (up to approximately 4-fold), macrophage chemoattractant protein-1 (up to approximately 4-fold), and osteopontin (up to approximately 13-fold) mRNA expression. Eplerenone attenuated proinflammatory molecule expression in the rat heart and subsequent vascular and myocardial damage. Thus aldosterone and salt treatment in uninephrectomized rats led to severe hypertension and the development of a vascular inflammatory phenotype in the heart, which may represent one mechanism by which aldosterone contributes to myocardial disease.
Authors:
Ricardo Rocha; Amy E Rudolph; Gregory E Frierdich; Denise A Nachowiak; Beverly K Kekec; Eric A G Blomme; Ellen G McMahon; John A Delyani
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  283     ISSN:  0363-6135     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2002 Nov 
Date Detail:
Created Date:  2002-10-17     Completed Date:  2002-11-22     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H1802-10     Citation Subset:  IM    
Affiliation:
Division of Cardiovascular and Metabolic Diseases, Pharmacia Corporation, Skokie, IL 60077, USA.
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MeSH Terms
Descriptor/Qualifier:
Aldosterone / pharmacology*
Animals
Blood Pressure
Chemokine CCL2 / genetics
Coronary Vessels / drug effects*,  immunology*
Cyclooxygenase 2
Endomyocardial Fibrosis / immunology,  pathology
Gene Expression / immunology
Hypertension / immunology,  pathology
Immunohistochemistry
In Situ Hybridization
Intercellular Adhesion Molecule-1 / analysis
Isoenzymes / genetics
Male
Myocardium / chemistry,  immunology,  pathology
Osteopontin
Phenotype
Prostaglandin-Endoperoxide Synthases / genetics
Rats
Rats, Sprague-Dawley
Sialoglycoproteins / analysis,  genetics
Spironolactone / analogs & derivatives*,  pharmacology
Vascular Cell Adhesion Molecule-1 / analysis
Vasculitis / chemically induced*,  immunology,  pathology
Chemical
Reg. No./Substance:
0/Chemokine CCL2; 0/Isoenzymes; 0/Sialoglycoproteins; 0/Spp1 protein, rat; 0/Vascular Cell Adhesion Molecule-1; 0/eplerenone; 106441-73-0/Osteopontin; 126547-89-5/Intercellular Adhesion Molecule-1; 52-01-7/Spironolactone; 52-39-1/Aldosterone; EC 1.14.99.1/Cyclooxygenase 2; EC 1.14.99.1/Prostaglandin-Endoperoxide Synthases
Comments/Corrections
Comment In:
Am J Med. 2003 Aug 15;115(3):250   [PMID:  12935835 ]

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