Depletion and accumulation of potassium in the extracellular clefts of cardiac Purkinje fibers during voltage clamp hyperpolarization and depolarization

1977 ◽  
Vol 368 (1-2) ◽  
pp. 19-31 ◽  
Author(s):  
Clive Marc Baumgarten ◽  
Gerrit Isenberg
1985 ◽  
Vol 249 (1) ◽  
pp. H108-H121
Author(s):  
J. M. Jaeger ◽  
W. R. Gibbons

Two outward currents, IX1 and IX2, are thought to be activated by depolarization of the Purkinje fiber. One of these, IX1, is presently believed to play a critical role in repolarization of the action potential. The IX currents were originally analyzed in voltage-clamp experiments in sheep Purkinje fibers. These experiments were designed to minimize interference by other currents, and it was assumed that changes of the net current were produced entirely by the IX currents. We have tried to repeat the original experiments and the analysis that led to acceptance of the existence and roles of the IX currents, without success. Moreover, tests of how membrane current should behave if the IX current hypothesis is correct did not give satisfactory results. Our data suggest the original conclusions about IX1 and IX2 may need substantial revision.


1977 ◽  
Vol 70 (2) ◽  
pp. 149-169 ◽  
Author(s):  
C M Baumgarten ◽  
G Isenberg ◽  
T F McDonald ◽  
R E Ten Eick

Voltage clamp hyperpolarization and depolarization result in currents consistent with depletion and accumulation of potassium in the extracellular clefts o cardiac Purkinje fibers exposed to sodium-free solutions. Upon hyperpolarization, an inward current that decreased with time (id) was observed. The time course of tail currents could not be explained by a conductance exhibiting voltage-dependent kinetics. The effect of exposure to cesium, changes in bathing media potassium concentration and osmolarity, and the behavior of membrane potential after hyperpolarizing pulses are all consistent with depletion of potassium upon hyperpolarization. A declining outward current was observed upon depolarization. Increasing the bathing media potassium concentration reduced the magnitude of this current. After voltage clamp depolarizations, membrane potential transiently became more positive. These findings suggest that accumulation of potassium occurs upon depolarization. The results indicate that changes in ionic driving force may be easily and rapidly induced. Consequently, conclusions based on the assumption that driving force remains constant during the course of a voltage step may be in error.


1984 ◽  
Vol 83 (5) ◽  
pp. 771-799 ◽  
Author(s):  
R T Falk ◽  
I S Cohen

Membrane current following prolonged periods of rapid stimulation was examined in short (less than 1.5 mm) canine cardiac Purkinje fibers of radius less than 0.15 mm. The Purkinje fibers were repetitively stimulated by delivering trains of depolarizing voltage clamp pulses at rapid frequencies. The slowly decaying outward current following repetitive stimulation ("post-drive" current) is eliminated by the addition of 10(-5) M dihydro-ouabain. The post-drive current is attributed to enhanced Na/K exchange caused by Na loading during the overdrive. Depolarizing voltage clamp pulses initiated from negative (-80 mV) or depolarized (-50 mV) holding potentials can give rise to post-drive current because of activation of tetrodotoxin-sensitive or D600-sensitive channels. The magnitude of the post-drive current depends on the frequency of voltage clamp pulses, the duration of each pulse, and the duration of the repetitive stimulation. The time constant of decay of the post-drive current depends on extracellular [K] in accordance with Michaelis-Menten kinetics. The Km is 1.2 mM bulk [K], [K]B. The mean time constant in 4 mM [K]B is 83 s. Epinephrine (10(-5) M) decreases the time constant by 20%. The time constant is increased by lowering [Ca]o between 4 and 1 mM. Lowering [Ca]o further, to 0.1 mM, eliminates post-drive current following repetitive stimulation initiated from depolarized potentials. The latter result suggests that slow inward Ca2+ current may increase [Na]i via Na/Ca exchange.


1986 ◽  
Vol 251 (5) ◽  
pp. H1056-H1061
Author(s):  
S. Terris ◽  
J. A. Wasserstrom ◽  
H. A. Fozzard

Isoproterenol reversibly depolarizes quiescent sheep cardiac Purkinje fibers, in contrast to its reported hyperpolarizing effect in many excitable tissues. The depolarization is inhibited by drugs that block beta 1-adrenergic receptors. Tetrodotoxin and verapamil have no effect on the isoproterenol-induced depolarization. Cesium reduced the isoproterenol-induced depolarization by 74%. The voltage dependency of activation of a current component called If, measured under voltage clamp, was shifted in the depolarizing direction by isoproterenol. No evidence was found to support the suggestion made for other tissues that the Na+-K+ pump is stimulated by isoproterenol. These data suggest that in quiescent sheep Purkinje fibers the isoproterenol-induced depolarization reflects activation of a pacemaker current.


1975 ◽  
Vol 65 (3) ◽  
pp. 367-384 ◽  
Author(s):  
W R Gibbons ◽  
H A Fozzard

A "slow" inward current (Is) has been identified in ventricular muscle and Purkinje fibers of several mammalian species. The two-microelectrode voltage clamp technique is used to examine some of the relationships between Is and contraction of the sheep cardiac Purkinje fiber. "Tails" of inward current occurring on repolarization and extrapolation of Is recovery each show that the Is system may not inactivate completely during prolonged depolarization. The rate of recovery of Is after a depolarization is slow, and when a train of 300-ms clamps (frequency 1 s-1) is begun after a rest, Is is larger for the first clamp than it is for succeedings clamps. For the first clamp after a rest, the thresholds for Is and tension are the same and there is a direct correlation between peak tension and peak Is for clamp voltages between threshold and minus 40 mV. After a clamp, however, the ability to contract recovers much more slowly than does Is. Therefore, since Is may occur under certain conditions without tension, the realtionship between Is and tension must be indirect. Calcium entering the cell via this current may replenish or augment an intracellular calcium pool.


1994 ◽  
Vol 80 (6) ◽  
pp. 1360-1368 ◽  
Author(s):  
David F. Stowe ◽  
Juraj Sprung ◽  
Lawrence A. Turner ◽  
John P. Kampine ◽  
Zeljko J. Bosnjak

1976 ◽  
Vol 231 (5) ◽  
pp. 1415-1420 ◽  
Author(s):  
P Posner ◽  
EL Farrar ◽  
CR Lambert

The effect of catecholamines over a wide range of concentrations was studied on 42K uptake and efflux, as well as on spontaneous rate in canine cardiac Purkinje fibers. Low levels of catecholamines (less than 10(-10) M epinephrine; less than 10(-9) M norepinephrine) decreased automaticity. This negative chronotropic effect was blocked by phentolamine and mimicked by phenylephrine. These low levels of epinephrine and norepinephrine also inhibited 42K uptake by Purkinje fibers but had no effect on 42K efflux. The inhibition of 42K uptake was blocked by phentolamine and verapamil and mimicked by phenylephrine. The data indicate an alpha-receptor-mediated negative response of rate and 42K uptake to low levels of catecholamine. The end result is discussed in terms of a competitive increase in the influx of Ca2+ rather than Na+ and an indirect inhibition of the Na+-K+ pump.


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