| Objective : To explore angiotensin II and telmisartan effects on electrophysiology characteristics in atrial myocytes and in vivo.To explain Renin Angiotensin System and its antagonist effects on possible electrophysiological mechanisms of atrial electrical remodeling and atrial fibrillation.Method: In vivo,32 canines was randomly divided into four groups:normal saline(control group), AngII group,telmisartan group, AngII+ telmisartan group(Combined group).The atrial effective refractory period(AERP) was measured at 3 different basic cycle length(BCL) (350ms,300ms,250ms) and 4 different time(0min, 15min, 30min, 60min). The AERP rate adapation, Inducibility and duration of atrial fibrillation was recorded simultaneously. In myocyte, single atrial myocyte of canine was obtained by enzymatic dissociation method with Langendorff apparatus. The whole cell patch-clamp recording technique was used to record the change of ICa-L and I-V curve by intervening of AngⅡ, telmisartan and AngⅡplus telmisartan respectively.Results: In vivo, compared with baseline(0min) AERP,AngII group were significantly shortened at 15min,30min at 3 different BCL on left atrium(LA) and right atrium(RA). (LA 350ms 130±4 vs 125±4 vs 119±4,300ms 126±3 vs 119±2 vs 113±5,250ms 115±4 vs 109±2 vs 102±4 RA 350ms 134±7 vs 128±5 vs 120±7,300ms 129±7 vs 122±5 vs 112±8,250ms 114±5 vs 108±2 vs 103±4)(P<0.05).At 60min, AERP recovered to the level comparable to baseline value(P>0.05).The AERP were no significant changes in other three groups at different BCL and time on LA or RA.Physiological rate adapation of AERP still remained in all the group duing the whole experimental session. The inducibility of AF is higher in AngII group than the other groups.The highest of the inducibility of AF is at the 15 min,the mean duration is 24.3s.In myocyte,AngII group significantly increased the peak density of ICa-L(P<0.05),but telmisartan and combined group had no significant effects on the peak density of ICa-L.The I-V curve of ICa-L were no change in each group.Conclusion: AngⅡhad directly electrophysiological effects on AERP as well as telmisartan could antagonist in vivo.AngII could change the channel by increased the peak density of ICa-L in myocyte,but telmisartan could antagonist at the level of angiotensin receptor.AngII could induce the atrial electrical remodeling(AER) both in vivo and in myocyte. |
