Standard microelectrode techniques were used to study the effects of captopril (1, 10 and 100 microM) on action potentials recorded from guinea-pig ventricular cells and sinoatrial node cells. 2. Captopril had no effect on the maximum rate of depolarization (Vmax) of ventricular action potentials in cells exposed to either normal Locke solution or 'simulated ischaemic' solution (K1 11.2 mM; pH-6.4; PO2 less than 80 mmHg), nor was there any augmentation of the normal small decline in Vmax with increasing stimulation rate (range of interstimulus intervals = 2400 ms to 300 ms). 3. Captopril had no effect on the duration of ventricular action potentials, nor did it alter the shortening seen on exposure to simulated ischaemia. 4. Captopril did not alter spontaneous sinus cycle length or any recorded parameter of sinus node action potentials. 5. It is concluded that any antiarrhythmic effects observed during clinical use of captopril are most unlikely to be due to direct actions of the drug on cardiac cell membrane properties.
