Effects of angiotensin converting enzyme inhibitor on the expression of angiotensin converting enzyme 2 in atrium of patients with atrial fibrillation.
- Author:
Xiao-sheng HU
1
;
Xu-dong XIE
;
Xing-xiang WANG
;
Chun-lai ZENG
;
Yi-ming NI
;
Guo-wei YU
;
Jun-zhu CHEN
Author Information
- Publication Type:Journal Article
- MeSH: Adult; Aged; Angiotensin-Converting Enzyme Inhibitors; therapeutic use; Atrial Fibrillation; drug therapy; metabolism; Female; Heart Atria; metabolism; Humans; Male; Middle Aged; Mitogen-Activated Protein Kinase 1; metabolism; Mitogen-Activated Protein Kinase 3; metabolism; Peptidyl-Dipeptidase A; metabolism; RNA, Messenger; metabolism; Signal Transduction
- From: Chinese Journal of Cardiology 2007;35(7):625-628
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the expression of angiotensin converting enzyme 2 (ACE2) and the changes treated with angiotensin converting enzyme inhibitor (ACEI), and its signal transduction pathway.
METHODSAtrial tissues were obtained from 47 patients with RHD undergoing cardiac surgery. The mRNA of ACE2 and ACE were semi-qualified by RT-PCR and normalized to the gene beta-actin. Western blot analysis was employed to examine the expressions of ACE2, ACE, ERK1/2 and phosphorylated ERK (pERK1/2). The atrial tissue angiotensin II (Ang II) content was determined by radioimmunoassay detection.
RESULTSThe expression of ACE2 was significantly decreased (P < 0.05), the expression of ACE and pERK1/2 were significantly increased (P < 0.05), and the level of atrial tissue Ang II was significantly increased in patients with chronic atrial fibrillation group (CAF) compared with sinus rhythm group (SR) (P < 0.05). Compared with CAF patients treated without ACEI, the expression of ACE2 significantly increased (P < 0.01), and the relative activity of ERK1/2 significantly decreased (P < 0.05), whereas the expression of ACE and the level of atrial tissue Ang II remained unchanged in CAF patients treated with ACEI.
CONCLUSIONSThe study suggested that the dysequilibrium of ACE/ACE2 might play an important role in the process of atrial fibrillation, which may be related to the activation of ERK1/2 pathway. The clinical effect of long-term treatment of ACEI maybe associated with elevated ACE2 expression but not ACE expression.