Norepinephrine, calcium, and discharge rate interact to modulate potassium uptake in cardiac Purkinje fibers through multiple mechanisms.
Should not yet change arrhythmia management; leaves open norepinephrine-calcium-rate effects on Purkinje K+ handling in vivo.
We studied the effect of norepinephrine, calcium concentration, and rate of discharge in the presence of different [Ca2+]0 on radioactive potassium movements in cardiac Purkinje fibers. The following results were obtained: (1) norepinephrine increases potassium uptake in quiescent fibers and in fibers driven at constant rate, but more in the latter; (2) norepinephrine also increases potassium uptake in quiescent fibers depolarized at the plateau; (3) increasing [Ca2+]0 increases potassium uptake in fibers driven at constant rate; (4) increasing [Ca2+]0 may decrease K+ uptake in quiescent fibers; (5) increasing [Ca2+]0 decreases the rate of loss of tissue radioactivity in quiescent fibers and increases it in a driven fiber; (6) increasing the driving rate increases potassium uptake in low and high [Ca2+]0; (7) high [Ca2+]0 increases K+ uptake, especially at low rates; (8) norepinephrine is less effective in increasing K+ uptake in the presence of a high [Ca2+]0. We conclude that: (a) norepinephrine increases potassium uptake by different mechanisms; (b) calcium affects potassium movements when it is allowed to enter the cell, presumably by affecting potassium conductance; (c) the effect of an increased rate of discharge on K+ uptake may involve stimulation of active K+ uptake and may include a calcium-dependent component which is largest at high [Ca2+]0 and a slow rate of drive; (d) simultaneous application of two interventions results in a summation that is smallest when one of the mechanisms is already substantially activated.
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Musso et al. (1978) studied this question.
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