OBJECTIVE: To investigate the mRNA and protein expression of mineralocorticoid receptor (MR) and 11-beta-hydroxysteroid dehydrogenase type 2 (11betaHSD2), which plays a crucial role in the human heart to confer specificity on MR, in patients with chronic atrial fibrillation. METHODS: Twenty-five patients of rheumatic heart valve disease, 12 with sinus rhythm, and 13 with chronic atrial fibrillation for 6 months or over, underwent transthoracic echocardiography and mitral/aortic valve replacement operation during which right atrial lateral wall tissue samples were obtained and left atrial lateral wall tissue samples were obtained from 14 of them in addition. Realtime quantitative PCR was used to determine the mRNA expression of MR and 11betaHSD2 and Western blotting was employed to detect the protein expression of MR and 11betaHSD2 in the atrial myocardium. RESULTS: The left atrial diameters increased markedly in the atrial fibrillation group as compared to the sinus rhythm group (P < 0.01). The mRNA expression of MR in the right atrium of the patients with atrial fibrillation was 5.37 +/- 1.15, significantly higher than that of the patients with sinus rhythm (2.67 +/- 1.09, P < 0.01), the mRNA expression of MR in the left atrium of the patients with atrial fibrillation was 5.19 +/- 1.14, significantly higher than that of the patients with sinus rhythm (270 +/- 0.82, P < 0.01). The mRNA expression of 11betaHSD2 in the right atrium of the patients with atrial fibrillation was 0.86 +/- 0.14, significantly higher than that of the patients with sinus rhythm (0.33 +/- 0.12, P < 0.01), and the mRNA expression of 11betaHSD2 in the left atrium of the patients with atrial fibrillation was 0.95 +/- 0.15, significantly higher than that of the patients with sinus rhythm (0.37 +/- 0.10, P < 0.01). The protein expression of MR in the right atrial tissue of the patients with atrial fibrillation was 1.65 +/- 0.72, significantly higher than that of the patients with sinus rhythm (0.86 +/- 0.33, P < 0.01); and the protein expression of MR in the left atrial tissue of the patients with atrial fibrillation was 1.72 +/- 0.62, significantly higher than that of the patients with sinus rhythm (0.97 +/- 0.37a, P < 0.05). The protein expression of 11betaHSD2 in the right atrial tissue of the patients with atrial fibrillation was 1.18 +/- 0.64, significantly higher than that of the patients with sinus rhythm (0.71 +/- 0.21, P < 0.05); and the protein expression of 11betaHSD2 in the left atrial tissue of the patients with atrial fibrillation was 1.36 +/- 0.58, significantly higher than that of the patients with sinus rhythm (0.85 +/- 0.15, P < 0.05). The mRNA expression and protein expression of MR and 11betaHSD2 were not significantly different between the left atria and right atria both in the fibrillation and sinus groups (all P > 0.05). CONCLUSION: The mRNA expression and protein expression of MR and 11betaHSD2 are upregulated in atrial fibrillation and aldosterone antagonists may be effective to arrest the development of sustained atrial fibrillation.
OBJECTIVE: To investigate the mRNA and protein expression of mineralocorticoid receptor (MR) and 11-beta-hydroxysteroid dehydrogenase type 2 (11betaHSD2), which plays a crucial role in the human heart to confer specificity on MR, in patients with chronic atrial fibrillation. METHODS: Twenty-five patients of rheumatic heart valve disease, 12 with sinus rhythm, and 13 with chronic atrial fibrillation for 6 months or over, underwent transthoracic echocardiography and mitral/aortic valve replacement operation during which right atrial lateral wall tissue samples were obtained and left atrial lateral wall tissue samples were obtained from 14 of them in addition. Realtime quantitative PCR was used to determine the mRNA expression of MR and 11betaHSD2 and Western blotting was employed to detect the protein expression of MR and 11betaHSD2 in the atrial myocardium. RESULTS: The left atrial diameters increased markedly in the atrial fibrillation group as compared to the sinus rhythm group (P < 0.01). The mRNA expression of MR in the right atrium of the patients with atrial fibrillation was 5.37 +/- 1.15, significantly higher than that of the patients with sinus rhythm (2.67 +/- 1.09, P < 0.01), the mRNA expression of MR in the left atrium of the patients with atrial fibrillation was 5.19 +/- 1.14, significantly higher than that of the patients with sinus rhythm (270 +/- 0.82, P < 0.01). The mRNA expression of 11betaHSD2 in the right atrium of the patients with atrial fibrillation was 0.86 +/- 0.14, significantly higher than that of the patients with sinus rhythm (0.33 +/- 0.12, P < 0.01), and the mRNA expression of 11betaHSD2 in the left atrium of the patients with atrial fibrillation was 0.95 +/- 0.15, significantly higher than that of the patients with sinus rhythm (0.37 +/- 0.10, P < 0.01). The protein expression of MR in the right atrial tissue of the patients with atrial fibrillation was 1.65 +/- 0.72, significantly higher than that of the patients with sinus rhythm (0.86 +/- 0.33, P < 0.01); and the protein expression of MR in the left atrial tissue of the patients with atrial fibrillation was 1.72 +/- 0.62, significantly higher than that of the patients with sinus rhythm (0.97 +/- 0.37a, P < 0.05). The protein expression of 11betaHSD2 in the right atrial tissue of the patients with atrial fibrillation was 1.18 +/- 0.64, significantly higher than that of the patients with sinus rhythm (0.71 +/- 0.21, P < 0.05); and the protein expression of 11betaHSD2 in the left atrial tissue of the patients with atrial fibrillation was 1.36 +/- 0.58, significantly higher than that of the patients with sinus rhythm (0.85 +/- 0.15, P < 0.05). The mRNA expression and protein expression of MR and 11betaHSD2 were not significantly different between the left atria and right atria both in the fibrillation and sinus groups (all P > 0.05). CONCLUSION: The mRNA expression and protein expression of MR and 11betaHSD2 are upregulated in atrial fibrillation and aldosterone antagonists may be effective to arrest the development of sustained atrial fibrillation.