Effects of XXXX on the action potential duration as modified by catecholamine-releasing action in @entity840 papillary muscles.

@entity5128 @entity1041 @entity1063 @entity840
The mechanism whereby @entity5128 ion ( @entity1041 ) prolongs the action potential (AP) was examined by standard microelectrode techniques in papillary muscles isolated from nonreserpinized and reserpinized @entity840 hearts. First, effects of 5 and 10 mmol/l @entity1041 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 @entity1041 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. @entity1041 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 @entity1041 -treated AP duration to control one was almost the same at all stimulation rates. @entity1041 slowed the recovery process of AP duration in the nonreserpinized preparations, but not in the reserpinized ones. @entity1041 had no effects on the recovery processes of Vmax and overshoot in both preparations. These results suggest that: @entity1041 modifies its intrinsic prolonging action of the AP by releasing @entity1063 from sympathetic nerve terminals; @entity1041 prolongs the AP by reducing the time-independent outward current rather than the time-dependent outward current; and a @entity1041 -sensitive current does not effectively contribute to the total ionic current at the time of Vmax.
