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Local Aldosterone Level In Atria, Mineralocorticoid Receptor And Atrial Structural Remodeling In Patients With Atrial Fibrillation

Posted on:2008-05-11Degree:DoctorType:Dissertation
Country:ChinaCandidate:D A PeiFull Text:PDF
GTID:1114360218458803Subject:Internal Medicine
Abstract/Summary:PDF Full Text Request
Objective: To investigate local aldosterone in atria, mineralocorticoid receptor (MR) and atrial structural remodeling in patients with atrial fibrillation (AF). Methods: Twenty-five patients with rheumatic heart valve disease, 12 with sinus rhythm and 13 with AF (AF≥6 months), underwent valve replacement operation, and right and left atrial wall tissue samples were obtained simultaneously from these patients. Radioimmunoassay were used to determine aldosterone, and collagen volume fraction and collagen subtype distribution were analyzed by VG staining and immunohistochemistry staining respectively. The expression of aldosterone synthase CYP11B2, MR and 11-beta-hydroxysteroid dehydrogenase type 2 (11βHSD2) were determined by using Realtime PCR and Western blot. Results: Atrial extracellular matrix remodeling was associated with the increasing aldosterone in atrial tissue along with upregulation of CYP11B2. Compared with that of sinus rhythm, the expression of MR and 11βHSD2 also were increased significantly in AF. But collagen distribution, aldosterone, MR, 11βHSD2 and CYP11B2 were found to be no difference between left atria and right atria both in AF and sinus groups. Conclusions: Atrial structural remodeling during AF was manifested by increased local aldosterone level in atria along with upregulation of CYP11B2. The upregulation of MR and 11βHSD2 may mediate atrial extracellular matrix remodeling. These findings suggested that aldosterone antagonists may be effective against atrial structural remodeling and the development of sustained AF.
Keywords/Search Tags:Atrial fibrillation, Atrial remodeling, Aldosterone, Collagen, Aldosterone synthase CYP11B2, Mineralocorticoid receptor, 11-beta-hydroxysteroid dehydrogenase type 2
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