Slow inward current and action potential in cardiac Purkinje fibres

1971 ◽  
Vol 323 (3) ◽  
pp. 204-218 ◽  
Author(s):  
M. Vitek ◽  
W. Trautwein
Keyword(s):  
Action Potential ◽  
Slow Inward Current ◽  
Purkinje Fibres ◽  
Inward Current ◽  
Cardiac Purkinje Fibres

The effects of sodium pump activity on the slow inward current in sheep cardiac Purkinje fibres

1982 ◽  
Vol 214 (1195) ◽  
pp. 249-262 ◽  
Keyword(s):  
Ion Concentration ◽  
Slow Inward Current ◽  
Purkinje Fibres ◽  
Inward Current ◽  
Na Pump ◽  
Pump Activity ◽  
External Site ◽  
K Concentration ◽  
Low K ◽  
Cardiac Purkinje Fibres

The effects of Na pump activity on the slow inward current, I si , magnitude and twitch tension were investigated in sheep cardiac Purkinje fibres. A two-microelectrode voltage-clamp method was used, tension being measured simultaneously. Na pump activity was lowered either by reducing the extracellular K concentration, [K] o , or by applying the cardiotonic steroid strophanthidin. Reduction of [K] o from 4 to 0 mM leads to time-dependent increases in I si magnitude and twitch tension. The increases of I si and tension could be reversed by adding Tl, Rb, Cs or NH 4 ions to the K-free superfusate. The actions of these ions are attributed to the known ability of these cations to activate the external site of the Na pump. This conclusion is supported by the observation that such activator cations do not reverse the increases in I si and tension produced by strophanthidin. We conclude that the effects of low [K] o on I si are mediated by Na pump inhibition. Similarly the Na pump inhibition produced by strophanthidin increases I si and tension, although, in this case, other mechanisms may also contribute. Measurements of the activity of the electrogenic Na pump show that elevated intracellular Na ion concentration secondary to Na pump inhibition and not the instantaneous Na pump turnover rate mediates the increase in I si magnitude.

Effects of ischemic conditions and reperfusion on depolarization-induced automaticity

1988 ◽  
Vol 255 (5) ◽  
pp. H992-H999 ◽  
Author(s):  
R. Mohabir ◽  
G. R. Ferrier
Keyword(s):  
Membrane Potential ◽  
Action Potential ◽  
Action Potentials ◽  
Cycle Length ◽  
Slow Inward Current ◽  
Potential Range ◽  
Ischemia And Reperfusion ◽  
Slow Response ◽  
Inward Current ◽  
High Membrane Potential

The inducibility of slow-response automaticity was assessed during ischemic conditions and reperfusion by application of extracellular current. Isolated canine Purkinje fibers were depolarized to membrane potentials less than -65 mV to elicit depolarization-induced automaticity (DIA). Ischemic conditions increased the cycle length of DIA and, in some tissues, prevented sustained DIA or completely abolished DIA. The magnitude of depolarization required to elicit DIA also increased. Inhibition of DIA occurred at a time when action potential plateaus were abbreviated. The effect of reperfusion on DIA was biphasic. Initial reappearance of DIA was followed by inhibition and reduction of the membrane potential range over which DIA could be elicited. Plateaus of action potentials initiated at high membrane potential were abbreviated at this time. DIA returned again as reperfusion effects dissipated. Phasic changes in the inducibility of DIA may represent changes in availability of the slow inward current and may regulate the timing and types of arrhythmic activity occurring with ischemia and reperfusion.

The toxic effects of ouabain: A voltage-clamp study

1982 ◽  
Vol 60 (9) ◽  
pp. 1153-1159 ◽  
Author(s):  
Y. Deslauriers ◽  
E. Ruiz-Ceretti ◽  
O. F. Schanne ◽  
M. D. Payet
Keyword(s):  
Action Potential ◽  
Voltage Clamp ◽  
Sodium Current ◽  
Negative Inotropic Effect ◽  
Slow Inward Current ◽  
Inward Current ◽  
Toxic Concentration ◽  
Voltage Curve ◽  
Current Voltage Curve ◽  
High Concentrations

The electrophysiologic effects of a toxic concentration of ouabain (10−5 M) were studied in frog atrial trabeculae. The toxic concentration was determined by the appearance of a negative inotropic effect and an increase in basal tension. Current- and voltage-clamp measurements were performed. Ouabain did not alter the passive electrical properties of the preparation. Under current-clamp conditions the membrane depolarized and the action potential amplitude as well as its maximum rate of rise decreased. The current–voltage curve for the fast inward current was shifted toward more positive potentials and the maximum sodium current decreased. The maximum sodium conductance was also reduced. The process of reactivation of the fast inward current was accelerated. The slow inward current and the maximum slow conductance also decreased under ouabain. These effects could explain the negative inotropic action of high concentrations of glycosides, as well as the action potential changes observed by several investigators. They also help to understand the arrhythmogenic effects of high concentrations of digitalis.

Slow inward current may produce many results attributed to IX1 in cardiac Purkinje fibers

1985 ◽  
Vol 249 (1) ◽  
pp. H122-H132
Author(s):  
J. M. Jaeger ◽  
W. R. Gibbons
Keyword(s):  
Action Potential ◽  
Outward Current ◽  
Purkinje Fiber ◽  
Slow Inward Current ◽  
Channel Blockers ◽  
Inward Current ◽  
Purkinje Fibers ◽  
Cardiac Purkinje Fibers ◽  
Current Voltage ◽  
Current Voltage Relation

We have tried to answer two fundamental questions concerning the outward current IX1 of cardiac Purkinje fibers. 1) Is it possible that current changes identified as arising from IX1 in voltage-clamp experiments are actually manifestations of changes in the slow inward current (Isi); and 2) is IX1 in fact required to produce the electrical phenomena attributed to it? Isi behavior and the role of IX1 were explored using computer simulation. The Isi model produced current changes during depolarizations and hyperpolarizations from depolarized resting potentials like those attributed to IX1. It also produced a component of "tail currents" that behaved like IX1. If these current changes were analyzed, assuming that an outward current is responsible, the resulting kinetics and current voltage relation would be very similar to the kinetics and current voltage relation reported for IX1. Using the McAllister, Noble, and Tsien formulation of the Purkinje fiber action potential, we found that IX1 is not essential for repolarization of the reconstructed action potential nor is it needed to reproduce interval duration effects and the effects of applied current in that model. Data suggesting that calcium channel blockers reduce IX1 and that catecholamines increase IX1 may be explained as arising from changes in Isi. Thus many manifestations of IX1 can be explained as arising from unanticipated behavior of Isi, and IX1 does not necessarily play a key role in generating Purkinje fiber electrical activity.

Tl+-Ions: Comparison of the Effects on the Slow Inward Current and Contractility of Ventricular Tissues

1982 ◽  
Vol 37 (10) ◽  
pp. 1015-1022 ◽  
Author(s):  
J. Wiemer ◽  
R. Ziskoven ◽  
C. Achenbach
Keyword(s):  
Voltage Clamp ◽  
Current System ◽  
Slow Inward Current ◽  
Initial Increase ◽  
Purkinje Fibres ◽  
Cardiac Tissues ◽  
Inward Current ◽  
Current Voltage ◽  
Apparent Relationship ◽  
Time Courses

To conclude our investigation of thallium effects on cardiac tissues, we studied the slow inward current of sheep cardiac Purkinje fibres exposed to 10-7 to 10-5 ᴍ Tl+ for extended periods of up to 80 min. Our previous results had suggested a possible involvement of the slow inward current during thallium intoxication: a) the modification of contractility staircases observed during thallium exposure, b) action potential recordings of ventricular muscle, c) changes in spontaneous beating in sino-atrial preparations. The thallium levels chosen were between those yielding strong positive inotropic transients and those producing a marked long­term decay of contraction force.The slow inward current was measured using a conventional two-microelectrode-technique and the standard voltage clamp protocol for this current system. The experimental work was restricted to the determination of d∞, the kinetics of activation of the slow inward current and of īsi, the current voltage relation of the current system. This was necessary since the effects of thallium were known to be short-lived and therefore frequent repeat runs of the voltage clamp program had to be performed in order to obtain the time courses of possible transient changes.The results showed that the slow inward current was first increased and then declined at the low concentration of 10-7 ᴍ Tl+. At 10-5 m Tl+ the initial increase was smaller, whereas the decay of the slow inward current proceeded to lower values. Comparison with contractility measure­ments at the same concentrations of thallium showed a distinct parallelism between changes of the slow inward current and myocardial contractility. Despite this apparent relationship, we do not conclude that the contractile events are primarily a result of changes of the slow inward current, since thallium does not seem to specifically alter the parameters of the slow inward current at the membrane level.

Participation of slow inward current in the Purkinje fiber action potential overshoot

1979 ◽  
Vol 237 (2) ◽  
pp. H204-H212
Author(s):  
L. Mary-Rabine ◽  
B. F. Hoffman ◽  
M. R. Rosen
Keyword(s):  
Action Potential ◽  
Action Potentials ◽  
Purkinje Fiber ◽  
Slow Inward Current ◽  
Inward Current ◽  
Slow Channel ◽  
Phase 0 ◽  
Relationship Of ◽  
The Relationship ◽  
Diastolic Potential

We used microelectrode techniques to study the relationship of canine Purkinje fiber membrane potential and the action potential (AP) overshoot. At the maximum diastolic potential, -93.0 +/- 0.5 (SE) mV, AP overshoot was +37.7 +/- 0.4 mV. There was a range of membrane potentials (MP) less negative than the maximum diastolic potential from which action potentials were elicited with an overshoot greater than the control. Starting at an MP of less than -78.7 +/- 0.4 mV, AP overshoot was less than control. A maximum overshoot of +40.2 +/- 0.4 mV occurred at an MP of -85.4 +/- 0.4 mV. The relationship of the maximum upstroke velocity (Vmax) of phase 0 depolarization to MP was sigmoidal. Peak Vmax, 497 +/- 13 V/s, occurred at MP greater than or equal to -89.3 +/- 0.5 mV. The increase in overshoot was enhanced as perfusate [Ca2+] increased and decreased as [Ca2+] decreased. Slow-channel blocking agents and tetrodotoxin (TTX) depressed the peak of the curve relating overshoot to MP. TTX also decreased Vmax. The effect of TTX on overshoot but not on Vmax was reversed with Ca2+, 8.1 mM. The increase in overshoot for action potentials initiated during the terminal part of phase 3 was due to a slow, delayed component of the upstroke and appears to result from the slow inward current.

Blockade of myocardial slow inward current at low pH

1977 ◽  
Vol 233 (3) ◽  
pp. C99-C103 ◽  
Author(s):  
S. Vogel ◽  
N. Sperelakis
Keyword(s):  
Electrical Stimulation ◽  
Action Potential ◽  
Low Ph ◽  
Slow Inward Current ◽  
Embryonic Chick ◽  
Slow Response ◽  
Na Current ◽  
Inward Current ◽  
Acid Ph ◽  
Subsequent Exposure

The effect of low pH on the slow cationic inward current was studied in isolated perfused embryonic chick ventricles (16-21 days old). In order to study the slow current, the fast Na+ current was inactivated by partial depolarization to about -40 mV by elevation of K+ (25 mM). Subsequent exposure of the tissue to catecholamines or methylxanthines allowed slowly rising overshooting electrical responses (the "slow response") with with accompanying contractions to be elicited by electrical stimulation. These slow responses are insensitive to tetrodotoxin and are Na+- and Ca2+-dependent. It was found that the isoproterenol- and caffeine-induced slow responses were abolished at about pH 6.1; 50% inhibition occurred at about pH 6.5. The rate of rise of the normal action potential, which is dependent on a fast Na+ current, was only slightly affected at these same pH levels; however, electromechanical uncoupling occurred, as expected from inhibition of the slow current. Therefore, the slow current was blocked at an acid pH that did not block the fast Na+ current.

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