The interrelationship of cesium, intracellular sodium activity, and pacemaker potential in cardiac Purkinje fibers

1990 ◽  
Vol 68 (9) ◽  
pp. 1236-1246 ◽  
Author(s):  
Giovanni Iacono ◽  
Mario Vassalle
Keyword(s):  
Membrane Potential ◽  
Intracellular Sodium ◽  
Resting Potential ◽  
Pacemaker Current ◽  
Purkinje Fibers ◽  
Sodium Activity ◽  
Diastolic Depolarization ◽  
Cardiac Purkinje Fibers ◽  
Myocardial Fibers

The actions of cesium (Cs) on intracellular sodium activity [Formula: see text], membrane potentials, and force were studied in sheep cardiac Purkinje and myocardial fibers superfused in vitro. In Purkinje fibers, Cs (2 mM) decreased diastolic depolarization, [Formula: see text] (−6.7%, p < 0.005), and force (−28.0%, p < 0.01). The effects of 4 and 8 mM Cs were more pronounced. In quiescent fibers, Cs (2–4 mM) also decreased [Formula: see text] (−17.3%, p < 0.005) and induced an initial hyperpolarization (+5.6 ± 1.3%, p < 0.005) followed by a return toward control. Diastolic depolarization was almost abolished by driving the fibers at 180/min (diastole was very short) but still Cs decreased [Formula: see text] (−15.4%). Tetrodotoxin decreased [Formula: see text] (−16.2%, p < 0.025) and reduced the Cs-induced fall in [Formula: see text] (−2.2%, p < 0.05). In zero [K]o, Cs decreased [Formula: see text] and caused repolarization. In 0.1 mM strophanthidin, Cs did not decrease [Formula: see text] any longer and affected the membrane potential little. In quiescent myocardial fibers, Cs (4 mM) decreased [Formula: see text] (−12.6%, p < 0.05) and transiently hyperpolarized (+2.1%). Rubidium (2 mM) decreased [Formula: see text] and resting potential in Purkinje fibers and in myocardial fibers and also decreased diastolic depolarization in Purkinje fibers. Thus, cesium and rubidium decrease [Formula: see text] and modify the membrane potential but not through a block of the inward pacemaker current If.Key words: rubidium, intracellular sodium activity, diastolic depolarization, tetrodotoxin, strophanthidin.

Acetylcholine increases intracellular sodium activity in sheep cardiac Purkinje fibers

1989 ◽  
Vol 256 (5) ◽  
pp. H1407-H1416
Author(s):  
G. Iacono ◽  
M. Vassalle
Keyword(s):  
Action Potential ◽  
Spontaneous Activity ◽  
Sodium Pump ◽  
Contractile Force ◽  
Intracellular Sodium ◽  
Resting Potential ◽  
Purkinje Fibers ◽  
Transmembrane Potentials ◽  
Sodium Activity ◽  
Cardiac Purkinje Fibers

The action of acetylcholine (ACh) on intracellular sodium activity (alpha iNa) was studied in sheep Purkinje fibers by means of a Na+-selective microelectrode technique while transmembrane potentials and contractile force were simultaneously recorded. In quiescent fibers, 10(-4) to 10(-5) M ACh shifted the resting potential to less negative values and increased alpha iNa from 5.57 +/- 0.21 to 6.45 +/- 0.35 mM (+15.8%, P less than 0.005). In other experiments, ACh induced a depolarization that initiated spontaneous activity. In fibers driven at 60 beats/min, ACh prolonged the action potential, increased alpha iNa from 7.98 +/- 0.15 to 9.36 +/- 0.3 mM (+17.29%, P less than 0.005), and increased contractile force. Norepinephrine (10(-5) to 10(-6) M) increased contractile force and decreased alpha iNa, but in its presence ACh still increased force and alpha iNa and vice versa. Strophanthidin (10(-4) M) increased alpha iNa, and 3 x 10(-6) M propranolol and 10(-6) M atropine decreased alpha iNa. Both strophanthidin and atropine (but not propranolol) prevented the increase in alpha iNa by ACh. It is concluded that the ACh increases alpha iNa and contractile force through the inhibition of the sodium pump and that these actions are due to the activation of the muscarinic receptor and not to endogenously released norepinephrine.

Toxic effects of ouabain on Purkinje fibers and ventricular muscle fibers

1962 ◽  
Vol 203 (3) ◽  
pp. 433-439 ◽  
Author(s):  
Mario Vassalle ◽  
Johannes Karis ◽  
Brian F. Hoffman
Keyword(s):  
Muscle Fibers ◽  
Toxic Effects ◽  
Resting Potential ◽  
Ventricular Muscle ◽  
Purkinje Fibers ◽  
Diastolic Depolarization ◽  
Series Of Experiments ◽  
Time Required ◽  
Induced Changes

Toxic effects of ouabain on single Purkinje fibers and ventricular muscle fibers were investigated in vitro by microelectrode technique. Toxicity developed much earlier in the specialized conducting fibers and consisted of a progressively increasing rate of diastolic depolarization and a decrease of amplitude and duration of the action potential. The majority of Purkinje fiber preparations developed extrasystoles and rapid spontaneous rhythms. The resting potential was much decreased. The ouabain-induced changes in ventricular muscle fibers occurred much later than did changes in Purkinje fibers and consisted of a decrease in the plateau and in the amplitude of the action and resting potential. Spontaneous depolarization was not observed in muscle fibers. The effect of the rate of stimulation on the development of ouabain toxicity was studied in another series of experiments on driven and quiescent muscles. Signs of toxicity appeared earlier in the driven muscles than in duplicate quiescent muscles and, at faster rates of stimulation, the time required for the toxic changes was shortened.

scholarly journals Effect on Membrane Potential and Electrical Activity of Adding Sodium to Sodium-Depleted Cardiac Purkinje Fibers

1974 ◽  
Vol 64 (4) ◽  
pp. 473-493 ◽  
Author(s):  
Jay R. Wiggins ◽  
Paul F. Cranefield
Keyword(s):  
Membrane Potential ◽  
Electrical Activity ◽  
Resting Potential ◽  
Average Increase ◽  
Purkinje Fibers ◽  
Cardiac Purkinje Fibers ◽  
Sodium Extrusion

Canine cardiac Purkinje fibers exposed to Na-free solutions containing 128 mM TEA and 16 mM Ca show resting potentials in the range -50 to -90 mV; if the concentration of Na in the perfusate is raised from 0 to 4 to 24 mM, hyperpolarization follows. If the initial resting potential is low, the hyperpolarization tends to be greater; the average increase in the presence of 8 mM Na is 14 mV. Such hyperpolarization is not induced by adding Na to K-free solutions, is not seen in cooled fibers, or in fibers exposed to 10-3 M ouabain, nor is it induced by adding Li and thus may result from electrogenic sodium extrusion. Fibers exposed to Na-free solutions are often spontaneously active; if they are quiescent they often show repetitive activity during depolarizing pulses. Such spontaneous or repetitive activity is suppressed by the addition of Na. This suppression may or may not be related to the hyperpolarization.

Intracellular sodium ion activity: reliable measurement and stimulation-induced change in cardiac Purkinje fibers

1987 ◽  
Vol 65 (5) ◽  
pp. 954-962 ◽  
Author(s):  
Chin O. Lee ◽  
Wook B. Im ◽  
Jong K. Sonn
Keyword(s):  
Membrane Potential ◽  
Time Constant ◽  
Fast Response ◽  
Intracellular Sodium ◽  
Sodium Ion ◽  
Sodium Influx ◽  
Stimulation Rate ◽  
Purkinje Fibers ◽  
Cardiac Purkinje Fibers ◽  
Ion Activity

Recently Na+-selective microelectrodes (NaSM) have been used to measure quantitatively small changes in intracellular sodium ion activity [Formula: see text] and to determine a precise time course of comparatively rapid change in [Formula: see text]. In such studies, accurate measurement of [Formula: see text] requires the following criteria: (i) NaSM should have a fast response time and (ii) an NaSM and a conventional voltage microelectrode should measure the same membrane potential. These criteria were evaluated by measuring [Formula: see text] when membrane potential of cardiac Purkinje fibers was suddenly hyperpolarized and depolarized by changing stimulation rate. The NaSM coated with a conductive silver paint had fast response times so that rapid changes in [Formula: see text] could be reliably measured. The cardiac Purkinje fibers stimulated at a constant rate generated uniform membrane voltage and the NaSM and conventional microelectrode measured virtually the same membrane potential. This result is somewhat different from that reported under voltage-clamp condition by other investigators. The [Formula: see text] of the fibers increased as the stimulation rate was increased over the range of 0.5–3 Hz. In fibers stimulated at 1 Hz, cessation of stimulation was immediately followed by an exponential decline of [Formula: see text] with an average time constant of 53 ± 9 s (SD, n = 8), or rate constant of 0.020 ± 0.004/s. Restimulation of the fibers produced an exponential rise of [Formula: see text] with an average time constant of 65 ± 12 s (n = 8). Similar results were obtained in fibers stimulated at 2 Hz. The average rates of rise of [Formula: see text] after the onset of stimulations at 1 and 2 Hz were 1.0 and 1.5 mM/min, equivalent to increments in net sodium influx of 13.2 and 19.8 pmol∙cm−2∙s−1, respectively. The average maximum rate of [Formula: see text] rise produced by the application of 10−5 M strophanthidin to the fibers stimulated at 1 Hz was 1.3 ± 0.5 mM/min, equivalent to a net sodium influx of 17.2 pmol∙cm−2∙s−1.

Different forms of spontaneous discharge induced by strophanthidin in cardiac Purkinje fibers

1982 ◽  
Vol 243 (5) ◽  
pp. H767-H778
Author(s):  
S. Ishikawa ◽  
M. Vassalle
Keyword(s):  
Oscillatory Potentials ◽  
Spontaneous Discharge ◽  
Purkinje Fibers ◽  
Diastolic Depolarization ◽  
Cardiac Purkinje Fibers ◽  
High Calcium ◽  
Low Potassium ◽  
Slow Rhythm ◽  
Fast Rhythm

The effect of strophanthidin on spontaneous discharge in canine cardiac Purkinje fibers perfused in vitro was studied during periodic interruptions (pauses) of the electrical drive. The results show that 1) strophanthidin initially increases the slope of diastolic depolarization and thereby induces a slow rhythm that accelerates progressively during the pause and becomes faster during the increasing strophanthidin inotropy; 2) oscillatory potentials appear only when strophanthidin inotropy reaches its peak (or actually declines) and may cause either a few fast action potentials during the pause or a fast rhythm that eventually overcomes the driven beats; 3) the slow rhythm is eliminated by cesium; 4) the fast rhythm is eliminated by tetrodotoxin; and 5) oscillatory potentials caused by high calcium, norepinephrine, or low potassium are similarly affected by cesium or tetrodotoxin. It is concluded that strophanthidin enhances diastolic depolarization, thereby causing the slow rhythm, and induces oscillatory potentials, thereby causing the fast rhythm. Only the oscillatory potentials are related to calcium overload as determined by several different procedures.

Effect of norepinephrine on Na(+)-K+ pump and Na+ influx in sheep cardiac Purkinje fibers

1990 ◽  
Vol 258 (4) ◽  
pp. C713-C722 ◽  
Author(s):  
S. W. Chae ◽  
D. Y. Wang ◽  
Q. Y. Gong ◽  
C. O. Lee
Keyword(s):  
Steady State ◽  
Membrane Potential ◽  
Action Potential ◽  
Action Potential Duration ◽  
Relative Magnitude ◽  
Resting Membrane Potential ◽  
Pacemaker Current ◽  
Purkinje Fibers ◽  
Cardiac Purkinje Fibers ◽  
High K

Effects of norepinephrine and Ca+ on Na(+)-K+ pump and pacemaker current were investigated by simultaneous measurement of intracellular Na+ activity (aiNa) and membrane potential in driven (1 Hz) and quiescent sheep cardiac Purkinje fibers. Concurrently, twitch force was measured in driven fibers, in which norepinephrine (NE) produced a decrease in aiNa, a prolongation in action potential duration, and a hyperpolarization in diastolic membrane potential, Vdm. In contrast, in quiescent fibers, NE produced an increase in aiNa and a depolarization in resting membrane potential, Vm. The decrease in aiNa, prolongation in action potential duration, and hyperpolarization in Vdm produced by NE were blocked by 5 x 10(-6) M strophanthidin, presumably through inhibition of the Na(+)-K+ pump. The increase in aiNa and membrane depolarization caused by NE were abolished by high [K+]o or Cs+, presumably through inhibition of the pacemaker current, if. These results indicate that in driven fibers NE stimulates predominantly the Na(+)-K+ pump, producing a decrease in aiNa and that in quiescent fibers it increases predominantly if, producing an increase in aiNa. The effect of NE on driven and quiescent fibers differs because of the voltage dependence of if and perhaps the Na(+)-K+ pump. Consequently, the relative magnitude of the two opposing effects of NE on aiNa appears to be dependent on membrane potential. In quiescent fibers, Cs+ monotonically decreased aiNa to a steady-state value, while Cs+ hyperpolarized membrane potential and then slowly depolarized to a steady-state level, producing a transient hyperpolarization. In driven fibers, Cs+ decreased aiNa, shortened action potential duration, and depolarized Vdm. Cs+ decreased aiNa more in quiescent fibers than in driven fibers. The decrease in aiNa and hyperpolarization in membrane potential produced by Cs+ in quiescent fibers were abolished by depolarization induced by high K+ extracellular concentration (25.4 mM) but were not abolished or reduced by 5 x 10(-6) M strophanthidin. These results suggest that the decrease in aiNa and hyperpolarization in membrane potential by Cs+ are caused by blockage of if but not by stimulation of the Na(+)-K+ pump and that if is an important source of Na+ loading into cells.

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