RESUMO
Objective To investigate the activation of renin angiotensin system(RAS)in the chronic atrial fibrillation (AF)dogs and the effects of Captopril in the treatment of AF.Methods Twenty-six mongrel dogs were randomly divided into three groups:pacing group(n=11),treatment group(n=9)and control group(n=6).High frequency pacing (400 b/min)of the right atrial appendage was performed for 8 weeks in the pacing group and treatment group with permanent pacemaker.Pacing was not performed in the control group.In the treatment group,the dogs were given Captopfil orally 50 mg twice a day from 3 days before pacing to 8 weeks after pacing.Tissue samples were obtained from the atrial appendages and both the left and fight atria when dogs were killed.The level of anglotensinⅡ(AugⅡ)and the intracellular Ca~(2+) concentrations were assayed by radio-immunity and spectrocomparator.Results The atrial AugⅡconcentrations were (29.83?5.73)pg/ml,(13.23?3.15)pg/ml,(11.38?2.14)pg/ml in pacing,treatment and control group, respectively.Compared with control group,the atrial AugⅡconcentrations in pacing group were significantly increased(P＜0.01 ),but no significant differences were found between treatment group and control group(P＞0.05).The intracellular Ca~(2+) concentrations were(35.32?4.88)?g/mg,(25.44?4.19)?g/mg,(24.06?3.51)?g/mg in pacing,treatment and control group,respectively.IntraceUular Ca~(2+) concentrations were higher in pacing group than that in the other two groups(P＜0.01).But in treatment group,the intracellular Ca~(2+) concentrations were almost the same as that in the control group(P＞0.05).Conclusion Chronic high frequency pacing could significantly increase the level of the atrial AugⅡand intracellular Ca~(2+) concentrations.Captopril could inhibit the RAS activation and the intracellular calcium overload and might present a new component for the treatment of AF.