Effects of Angiotensin Ⅱ and ACE Inhibitor, Captopril on L-type Calcium Current and Sodium Current of Single Guinea Myocytes

徐延敏; 黄体钢; 陈元禄

摘要：Objectives To investigateeffect of AngⅡ, captopril on single guinea myocytes onL - type calcium current and sodium current. MethodsMembrane patch clamp whole cell recording tech-nique was used to investigate effect of angⅡ, captoprilon L- Ca maximum current density and sodium maxi-mum current density. Resutls AngⅡ increased themaximum current density compared with control afterpeffused 5 min, 357.7±219.7 Vs 279.5±240.5PA/PF, increase rate is 27.9 %, the shape of current- voltage relationship curve was unchanged, peaked at+ 10 my, indicated that angⅡ increased L- Ca cur-rent density in voltage -dependent. After perfusedwith captopril, captopril ± angⅡ 3, 5 rmin, L-Cacurrent was recorded, results suggest L - Ca maximumcurrent density decreased significantly compared withcontrol, in captopril group, 128.4 ± 92.6Vs286.2 ±89.7, 66.7 ±68.3Vs 286.2 ± 89.7, respectively, rateof inhibition is 55.1%, 76.6 %, respectively. L - Cacurrent further decreased in captopril perfused 5 mincompared with 3 rmin, 66.7 ± 68.3 Vs 128.4 ± 92.6,in captopril + angⅡ group, L- Ca current decreasedgreatly in 3, 5 min than control, 143.4 ± 117.6Vs267.7±141.4, 96.4±82.5 Vs 267.7+141.4, re-spectively, rate of inhibition is 46.4 %, 63.9 % re-spectively. We also investigated effect of captopril onNa current, which decreased significantly in 1 rmin and3 rmin compared with control, 939.1 ±319. 1 Vs1398.0 ± 144.6 PA/PF, 469.95±314.9 Vs 1398.0±144.6 PA/PF, respectively, rate of inhibition is32.8 %, 66. 3 %, respectively. Na current density de-creased significantly in 3 min compared with 1 min,469.9 ± 314.9 Vs 939. 1 ± 319. 1PA/PF, rate of in-hibition is 49.9 % . Conclusions Angiotensin Ⅱexerts increased maximum current density of L - Ca involtage dependent, captopril decreased maximum cur-rent density of L - Ca in voltage dependent, decreasedsodium maximum current density, which is the promi-nently antiarrhythmia mechanisms through inhibition ofangiotensin Ⅱ evoked calcium dependent transient in-ward current and calcium overload.