Premium
Angiotensin‐(1–7) Prevent Atrial Tachycardia Induced Sodium Channel Remodeling
Author(s) -
WANG XUEWEN,
LI GUANGPING
Publication year - 2014
Publication title -
pacing and clinical electrophysiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.686
H-Index - 101
eISSN - 1540-8159
pISSN - 0147-8389
DOI - 10.1111/pace.12427
Subject(s) - medicine , atrial fibrillation , sodium channel , angiotensin ii , atrial tachycardia , renin–angiotensin system , cardiology , endocrinology , tachycardia , sodium , receptor , catheter ablation , blood pressure , chemistry , organic chemistry
Background Activation of the renin‐angiotensin system plays an important role in atrial electrical remodeling; angiotensin‐(1–7) (Ang‐(1–7)) counterbalances the actions of angiotensin II. The aim of this study was to determine the effects of Ang‐(1–7) on cardiac sodium current (I Na ) in a canine model of atrial tachycardia. Methods Eighteen dogs were randomly assigned to sham, pacing, or pacing + Ang‐(1–7) groups (n = 6 in each group). Rapid atrial pacing (500 beats/min) was maintained for 2 weeks, while the dogs in the sham group were not paced. Ang‐(1–7) (6 μg/kg/h) was administered intravenously during pacing. Whole‐cell patch clamp techniques were utilized to record I Na from canine atrial myocytes. Reverse transcription‐polymerase chain reaction was used to assess possible underlying changes in cardiac Na + channels (Nav1.5). Results Our results showed that I Na density and expression of the Nav1.5 mRNA significantly decreased following pacing (P < 0.05 vs sham); however, the half‐activation voltage (V 1/2act ) and half‐inactivation voltage (V 1/2inact ) of I Na were not significantly altered (P > 0.05 vs sham). Ang‐(1–7) treatment significantly increased I Na densities and hyperpolarized V 1/2act without concomitant changes in V 1/2inact but have no effect on the expression of the Nav1.5 gene. Conclusions Ang‐(1–7) significantly increased I Na densities, which contributed to improving intraatrial conduction and decreasing the likelihood of atrial fibrillation maintenance.