Effects of tetraethylammonium on the action potential duration as modified by catecholamine-releasing action in guinea-pig papillary muscles.

The mechanism whereby tetraethylammonium ion (TEA) prolongs the action potential (AP) was examined by standard microelectrode techniques in papillary muscles isolated from nonreserpinized and reserpinized guinea-pig hearts. First, effects of 5 and 10 mmol/l TEA on steady-state AP parameters, i.e. the maximum rate of rise of AP (Vmax), AP amplitude, AP duration and resting potential, were examined at stimulation rates of 0.1 to 5 Hz. Second, effects of 5 and 10 mmol/l TEA on nonsteady-state AP parameters, i.e. the recovery processes of Vmax, AP duration and overshoot, were examined by introducing premature responses with various diastolic intervals between the basic stimulation rate of 0.1 Hz. TEA prolonged the AP more in the nonreserpinized preparations than in the reserpinized ones at all stimulation rates. In both preparations, this prolongation of the AP was greater at lower rates (0.1-1 Hz) than at higher rates (2-5 Hz), but the ratio of TEA-treated AP duration to control one was almost the same at all stimulation rates. TEA slowed the recovery process of AP duration in the nonreserpinized preparations, but not in the reserpinized ones. TEA had no effects on the recovery processes of Vmax and overshoot in both preparations. These results suggest that: TEA modifies its intrinsic prolonging action of the AP by releasing norepinephrine from sympathetic nerve terminals; TEA prolongs the AP by reducing the time-independent outward current rather than the time-dependent outward current; and a TEA-sensitive current does not effectively contribute to the total ionic current at the time of Vmax.