| Objective:To observe the effect of Angiotensin-(1-7) which through receptor Mas mediates endothelial nitric oxide synthase activation via Akt-dependent pathways on atrial electrical remodeling and the trend of atrial natriuretic peptide levels in atrial tissure.Methods:Fifty-six mongrel dogs were randomly assigned to sham group (AS group), paced group (AC group), paced+Ang-(1-7) group (AA group), paced+Ang-(1-7)+Mas inhibitor A-779group (AN group), paced+Ang-(1-7)+Akt inhibitor API-2group (AP group), paced+Ang-(1-7)+PI3K inhibitor Wort group (AW group) and paced+Ang-(1-7)+eNOS inhibitor L-NAME group (AL group). Right atrial pacing at600beats per minute was maintained for2hours. Six bipolar recording electrodes were sutured to sites of both atrial during experiments. Some index were measured, including atrial effective refractory period (AERP), rate adaptability, inducibility and duration of induced atrial fibrillation under different basic pacing cycle lengths (300,250and200ms). The concentrations of atrial natriuretic peptide (ANP) were measured by ELISA.Results:Compared with AS group, the values of AERP at6sites of AC group were shortened and maladaptation. In AC group the inducibility and duation of induced AF increased significantly than those of AS group (P<0.05). However, there were no differences in these parameters between AA and AS groups. Compared with AC group, AA group had a longer AERP, decreased maladaptation and decreased inducibility and duation of induced AF. Compared to AC group, no significant changes of those parameters were found in AN, AP, AW and AL groups. ANP was significantly higher in AA group than in AS and AC group. Exclusive of AA group, there were no differences of the ANP level in other6groups. Conelusion:Ang-(1-7) prevents tachycardia-induced acute atrial electrical remodeling in dogs and stimulates the release of ANP. The inhibitors of Ang-(1-7) signal transduction pathway make this effect unavailable. |
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