Aim: To study the direct effect of enalapril on cellular electrophysiology of myocardium.
Methods: Conventional microelectrodes technique was used to record the action potentials (AP) of guinea pig papillary muscles.
Results: Enalapril caused an increase of the AP amplitude (APA) and the resting potential (RP) in a concentration-dependent manner without any significant change of AP duration, Vmax and overshoot of AP. Superfusion of ouabain 0.5 mumol.L-1 reduced APA and RP, induced stable delayed after-depolarizations (DAD) at different basic cycle lengths (BCL) in a frequency-dependent manner. At BCL 200 ms, the amplitude of DAD was large enough to induce nonsustained triggered activity (TA). In additional presence of enalapril 10 mumol.L-1, the DAD amplitude at 500, 400, 300, and 200 ms were decreased from 5.3 +/- 2.3, 5.9 +/- 2.8, 7.4 +/- 2.1, and 8.9 +/- 1.3 to 2.6 +/- 0.7, 3.1 +/- 1.0, 3.7 +/- 1.5, and 5.3 +/- 1.1 (mV) respectively, all P < 0.01. The compensation intervals were increased in a similar frequency-dependent manner. The number of TA induced at BCL 200 ms was decreased from 3.6 +/- 0.7 to 0.8 +/- 0.2 (P < 0.05).
Conclusion: Enalapril directly inhibits DAD and TA induced by ouabain through increasing RP and APA, which may contribute to its anti-arrhythmic effect.