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Am J Physiol Heart Circ Physiol (June 27, 2002). doi:10.1152/ajpheart.01096.2001
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Articles in PresS, published online ahead of print June 27, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.01096.2001
Submitted on December 21, 2001
Accepted on June 26, 2002

Aldosterone Induces a Vascular Inflammatory Phenotype in the Rat Heart

Ricardo Rocha1, Amy E. Rudolph1, Gregory E. Frierdich1, Denise A. Nachowial1, Beverly K. Kekec1, Eric A. G. Blomme2, Ellen G. McMahon1, and John A. Delyani1*

1 Cardiovascular and Metabolic Disease, Pharmacia, Skokie, IL, USA
2 Global Toxicology, Pharmacia, Skokie, IL, USA

* To whom correspondence should be addressed. E-mail: john.a.delyani{at}pharmacia.com.

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 weeks and i) vehicle; ii) aldosterone infusion (0.75 µg/h); or iii) aldosterone infusion (0.75 µg/h) plus the selective aldosterone blocker, eplerenone (100 mg/kg/d). Aldosterone induced severe hypertension at 4 weeks (Systolic blood pressure (SBP): 210 ± 3 mm Hg vs. vehicle: 131 ± 2 mm Hg, P<0.001), which was partially attenuated by eplerenone (SBP: 180 ± 7 mm Hg, 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, histopathologic 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 ~4-fold), macrophage chemoattractant protein-1 (up to ~4-fold), and osteopontin (up to ~13-fold) mRNA expression. Eplerenone attenuated proinflammatory molecule expression in the rat heart and subsequent vascular and myocardial damage. Thus, aldosterone/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.




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