https://orcid.org/0000-0002-1658-7980
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Abstract
Purpose
Atrial remodeling takes part in the pathogenesis of atrial fibrillation (AF). Aliskiren, as a direct renin inhibitor, has been shown to exert protective effects against arrhythmia. The aim of this study was to investigate the potential role of aliskiren in atrial remodeling in a chronic intermittent hypoxia (CIH) rat model.
Methods
A total of 45 Sprague–Dawley rats were randomly assigned into three groups (n=15 per group): control group; CIH group; and CIH with aliskiren (CIH-A) group. CIH and CIH-A rats were subjected to CIH for 6 h per day for 4 weeks. Atrial fibrosis was evaluated using Masson’s trichrome staining. Electrophysiological tests were conducted in the isolated perfused hearts to assess the atrial effective refractory period and inducibility of AF. Atrial ionic remodeling was measured using the whole-cell patch-clamp technique, and Western blotting and real-time quantitative polymerase chain reactionwere performed to evaluate changes in ion channels.
Results
CIH induced obvious collagen deposition, and the abnormal fibrosis was significantly attenuated by aliskiren. The inducibility of AF was increased significantly in the CIH group compared with the control and CIH-A groups (23±24.5% vs 2.0±4.2% vs 5.0±7.0%, respectively; P<0.05). Compared with the control group, the densites of the calcium current (ICaL) and sodium current (INa) were reduced significantly in the CIH group (ICaL: −3.16±0.61 pA/pF vs −7.13±1.98 pA/pF; INa: −50.97±8.71 pA/pF vs −132.58±25.34 pA/pF, respectively; all P<0.05). Following intervention with aliskiren, the reductions in ICaL and INa were significantly improved, and the ionic modeling changes assessed at the mRNA and protein levels were also significantly improved.
Conclusion
CIH could alter atrial modeling and subsequently promote the occurrence and development of AF, which could be attenuated by treatment with aliskiren.
Disclosure
The authors declare no conflicts of interest for this work.