Angiotensin II receptor type 1 is upregulated in atrial tissue of patients with rheumatic valvular disease with atrial fibrillation

Abstract

The purpose of this study was to examine the changes in expression of angiotensin II receptor type 1/2 in left or right atrial tissue from patients with rheumatic valvular disease with or without atrial fibrillation. Atrial tissue samples were obtained from 39 patients with rheumatic mitral valve disease during cardiac surgery. Among these patients, there were 25 with atrial fibrillation and 14 with sinus rhythm. The level of angiotensin II receptor type 1 or type 2 mRNA transcription was measured by means of a semiquantitative reverse transcription-polymerase chain reaction technique. Expression of angiotensin II receptor type 1 or type 2 protein was detected by means of immunohistochemistry assay and Western blot analysis. The inner diameter of the left atrium was clearly enlarged in the atrial fibrillation group in comparison with that seen in the sinus rhythm group. The expression levels of both angiotensin II receptor type 1 mRNA and protein in the left atrial tissue were significantly increased in the patients with atrial fibrillation compared with those seen in patients with sinus rhythm (P < .05). Interestingly, the comparison of angiotensin II receptor type 2 expression levels in the left atrial tissue between these 2 groups is not statistically significant. In addition, the results of angiotensin II receptor type 1 or 2 expression in the right atrial tissue did not show any obvious change in the patients with atrial fibrillation versus those with sinus rhythm. Expression of angiotensin II receptor type 1 but not type 2 is highly upregulated only in the left atrial tissue of patients with rheumatic valvular disease with atrial fibrillation. This suggests that there is a possible pathophysiologic role of the renin-angiotensin system in patients with atrial fibrillation and that a series of effects mediated by the activation of angiotensin II receptor type 1 in the left atrial tissue might be one of the molecular mechanisms involved in the process of atrial remodeling in atrial fibrillation.