血管紧张素-（1-7）信号转导途径对犬急性心房电重构的影响

Objective: Angiotensin-(1-7) [Ang-(1-7)] through receptor Mas mediates endothelial nitric oxide synthase activation via Akt-dependent pathways.To observe the effect of different inhibitors of this pathway on atrial electrical remodeling. Methods: Thirty-five mongrel dogs were randomly assigned to AS(shame)、AC(control)、AA [paced+Ang-(1-7)],AN [paced+Ang-(1-7)+Mas inhibitor A-779],AP [paced+Ang-(1-7)+Akt inhibitor API-2],AW [paced+Ang-(1-7)+PI3K inhibitor Wort] and AL[paced+Ang-(1-7)+eNOS inhibitor L-NAME] groups.Right atrial pacing at 600 beats per minute was maintained for 2 hours.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 length(300,250and200ms). Results:Contrast with AS group，the values of AERP at 6 sites of AC group were shortened and maladaptation. In AC group the inducibility and duation of induced AF increased significantly than those of AS groups(P<0.05).Hower,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. Conclusion:Ang-(1-7) prevents tachycardia-induced acute atrial electrical remodeling in dogs and the inhibitors of Ang-(1-7) signal transduction pathway make this effect unavailable.?????