Membrane permeability during low potassium depolarization in sheep cardiac Purkinje fibers

1979 ◽  
Vol 237 (3) ◽  
pp. C156-C165 ◽  
Author(s):  
C. O. Lee ◽  
H. A. Fozzard
Keyword(s):  
Membrane Potential ◽  
Membrane Permeability ◽  
Resting Potential ◽  
Equilibrium Potential ◽  
Purkinje Fibers ◽  
Cardiac Purkinje Fibers ◽  
Low Potassium ◽  
Low K ◽  
Fiber Action ◽  
K Activity

Exposure of sheep Purkinje fibers to low [K]o leads to marked depolarization to a stable potential of about -40 mV. This level is equivalent to the plateau of the Purkinje fiber action potential. The low [K]o depolarization could be prevented by removal of [Na]o and was modified by tetrodotoxin. The membrane potential in the depolarized state was unresponsive to changes in [Cl]o or [Ca]o and it was poorly responsive to changes in [K]o between 0 and 2 mM. Repolarization was induced by decrease in [Na]o with a slope response of 30 mV/10-fold change in [Na]o. Average internal K activity (aK) in the resting state with a [K]o of 5 mM was 121.4 mM for a membrane potential of -80 mV. During low K depolarization aK was 119.7 mM with a membrane potential of -34 mV. The depolarization was therefore due to a change in membrane permeability, with little change in aK. Upon restoration of [K]o the fiber repolarized to values transiently more negative than the prior resting potential. These transient potentials were more negative than the K equilibrium potential (VK), if it is calculated assuming a uniform [K]o. The hyperpolarization was reduced by ouabain [10(-6)] or by low [Ca]o.

Quantitative relation of twitch and tonic tensions to intracellular Na+ activity in cardiac Purkinje fibers

1984 ◽  
Vol 247 (5) ◽  
pp. C478-C487 ◽  
Author(s):  
W. B. Im ◽  
C. O. Lee
Keyword(s):  
Membrane Potential ◽  
Linear Functions ◽  
Quantitative Relation ◽  
Purkinje Fibers ◽  
Average Value ◽  
Intracellular Na Activity ◽  
Cardiac Purkinje Fibers ◽  
Ion Activities ◽  
Model Equations ◽  
Low K

Quantitative relation of twitch and tonic tensions to intracellular Na ion was studied by describing model equations and measuring simultaneously the electrical, mechanical, and intracellular Na ion activities in electrically driven cardiac Purkinje fibers exposed to strophanthidin, tetrodotoxin (TTX), and varied [K+]0. In each experiment a plot of tension (T) vs. intracellular Na ion activity (aiNa) on logarithmic coordinates showed a good fit of the data to a single line described by the equation of T = beta (aiNa) gamma, in which beta and gamma represent the intercept and slope of the log T-log aiNa relation. Implication and average values of beta were presented. The average value of gamma obtained was 6.1 +/- 0.9 (SD, n = 8) in the experiments with strophanthidin (5 X 10(-7) - 10(-6) M) that somewhat depolarized transmembrane potential (Vm). The gamma value was 6.6 +/- 1.4 (n = 6) in the experiments with TTX (10(-6) - 5 X 10(-6) M) that shortened action potential duration. The gamma of 4.3 +/- 0.7 (n = 5) and 4.0 +/- 0.5 (n = 6) were obtained with the low [K+]0 of 1.0 and 2.0 mM, respectively, that hyperpolarized diastolic membrane potential by 12.7 +/- 6.3 mV (n = 5) and 13.7 +/- 2.4 mV (n = 6). The gamma value was 7.0 +/- 1.7 (n = 10) in the experiments with 8.1 mM [K+]0 that depolarized diastolic potential by 10.8 +/- 1.4 mV (n = 10). K+-free solution resulted in the gamma values of 6.0 +/- 0.9 (n = 6) for the twitch-aiNa relation and 5.3 +/- 1.4 (n = 9) for the tonic tension-aiNa relation. Except the experiments with the low [K+]0 the gamma values obtained are reasonably close to the value of 6.0 that is given on the basis of the 3Na-1Ca exchange and Ca2+-tension relation. In the experiments with the low [K+]0, the gamma values lower than 6.0 may be explained by the large hyperpolarization of diastolic membrane potential that could reduce intracellular calcium by means of the Na-Ca exchange. In conclusion, aiNa is a powerful determinant of twitch and tonic tensions which, in most instances, are linear functions of (aiNa)approximately 6.

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.

scholarly journals The effect of extracellular potassium on the intracellular potassium ion activity and transmembrane potentials of beating canine cardiac Purkinje fibers.

1977 ◽  
Vol 69 (4) ◽  
pp. 463-474 ◽  
Author(s):  
D S Miura ◽  
B F Hoffman ◽  
M R Rosen
Keyword(s):  
Equilibrium Potential ◽  
Extracellular Potassium ◽  
Purkinje Fibers ◽  
Transmembrane Potentials ◽  
Cardiac Purkinje Fibers ◽  
K Concentration ◽  
Range Of Values ◽  
Intracellular K Activity ◽  
Liquid Ion Exchanger ◽  
K Activity

We used open tip microelectrodes containing a K+-sensitive liquid ion exchanger to determine directly the intracellular K+ activity in beating canine cardiac Purkinje fibers. For preparations superfused with Tyrode's solution in which the K+ concentration was 4.0 mM, intracellular K+ activity (ak) was 130.0+/-2.3 mM (mean+/-SE) at 37 degrees C. The calculated K+ equilibrium potential (EK) was -100.6+/-0.5 mV. Maximum diastolic potential (ED) and resting transmembrane potential (EM) were measured with conventional microelectrodes filled with 3 M KCl and were -90.6+/-0.3 and -84.4+/-0.4 mV, respectively. When [K+]o was decreased to 2.0 mM or increased to 6.0, 10.0, and 16.0 mM, ak remained the same. At [K+]o=2.0, ED was -97.3+/-0.4 and Em -86.0+/-0.7 mV; at [K+]o=16.0, ED fell to -53.8+/-0.4 mV and Em to the same value. Over this range of values for [K+]o, EK changed from -119.0+/-0.3 to -63.6+/-0.2 mV. These values for EK are consistent with those previously estimated indirectly by other techniques.

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.

Beta-adrenergic actions on membrane electrical properties of dissociated smooth muscle cells

1988 ◽  
Vol 254 (3) ◽  
pp. C423-C431 ◽  
Author(s):  
H. Yamaguchi ◽  
T. W. Honeyman ◽  
F. S. Fay
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Electrical Properties ◽  
Smooth Muscle Cells ◽  
Input Resistance ◽  
Muscle Cells ◽  
Resting Potential ◽  
Equilibrium Potential ◽  
Dependent Manner ◽  
Beta Adrenergic

Studies were carried out to determine the effects of the beta-adrenergic agent, isoproterenol (ISO), on membrane electrical properties in single smooth muscle cells enzymatically dispersed from toad stomach. In cells bathed in buffer of physiological composition, the average resting potential was -56.4 +/- 1.4 mV (mean +/- SE, n = 35). The dominant effect of exposure to ISO was hyperpolarization. The hyperpolarization was apparent in all cells studied and averaged 11.6 +/- 1.2 mV (n = 27). In the majority of the cells, hyperpolarization was accompanied by a decreased input resistance (Rin). Often the change in resistance appeared to lag behind the change in membrane potential. The lack of coincident changes in membrane potential and resistance may reflect a superposition of the outward rectification properties of the membrane on beta-adrenergic-induced increases in ionic conductance. In about half of the cells, an initial small depolarization (3.1 +/- 0.3 mV, n = 14) was accompanied by a small but distinct increase in Rin (12 +/- 2.5%). When membrane potential was made more negative than the estimated equilibrium potential for K+ (EK) by injection of current, ISO also produced biphasic effects, an initial hyperpolarization which reversed to a sustained depolarization to a value (-90 mV) near the estimated EK. The hyperpolarization by ISO could be diminished in a time-dependent manner by previous exposure to ouabain. The inhibition by ouabain, however, appeared to be a fortuitous result of glycoside-induced positive shifts in EK. These observations indicate that the dominant electrophysiological effect of beta-adrenergic stimuli is to hyperpolarize the cell membrane.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Effect of acetylcholine on postjunctional membrane permeability in eel electroplaque.

1977 ◽  
Vol 70 (1) ◽  
pp. 23-36 ◽  
Author(s):  
N L Lassignal ◽  
A R Martin
Keyword(s):  
Field Equation ◽  
Membrane Potential ◽  
Membrane Permeability ◽  
Ionic Composition ◽  
Reversal Potential ◽  
Resting Potential ◽  
Constant Field ◽  
Free Solution ◽  
Positive Direction ◽  
External K

Acetylcholine (ACh) was applied iontophoretically to the innervated face of isolated eel electroplaques while the membrane potential was being recorded intracellularly. At the resting potential (about -85 mV) application of the drug produced depolarizations (ACh potentials) of 20 mV or more which became smaller when the membrane was depolarized and reversed in polarity at about zero membrane potential. The reversal potential shifted in the negative direction when external Na+ was partially replaced by glucosamine. Increasing external K+ caused a shift of reversal potential in the positive direction. It was concluded that ACh increased the permeability of the postjunctional membrane to both ions. Replacement of Cl- by propionate had no effect on the reversal potential. In Na+-free solution containing glucosamine the reversal potential was positive to the resting potential, suggesting that ACh increased the permeability to glucosamine. Addition of Ca++ resulted in a still more positive reversal potential, indicating an increased permeability to Ca++ as well. Analysis of the results indicated that the increases in permeability of the postjunctional membrane to K+, Na+, Ca++, and glucosamine were in the ratios of approximately 1.0:0.9:0.7:0.2, respectively. With these permeability ratios, all of the observed shifts in reversal potential with changes in external ionic composition were predicted accurately by the constant field equation.

Control of intracellular calcium by membrane potential in human melanoma cells

1993 ◽  
Vol 265 (6) ◽  
pp. C1501-C1510 ◽  
Author(s):  
B. Nilius ◽  
G. Schwarz ◽  
G. Droogmans
Keyword(s):  
Cell Proliferation ◽  
Membrane Potential ◽  
Intracellular Calcium ◽  
Reversal Potential ◽  
Melanoma Cells ◽  
Human Melanoma ◽  
Resting Potential ◽  
Equilibrium Potential ◽  
Patch Clamp Technique ◽  
Human Melanoma Cells

The modulation of intracellular calcium ([Ca2+]i) by the membrane potential was investigated in human melanoma cells by combining the nystatin-perforated patch-clamp technique with Ca2+ measurements. Voltage steps to -100 mV induced a rise in [Ca2+]i and a creeping inward current. These effects were absent in Ca(2+)-free solution and could be blocked by Ni2+ or La3+. Voltage ramps revealed a close correlation between [Ca2+]i and voltage, with the strongest voltage dependence around the resting potential. Long-lasting tail currents, closely correlated with the rise in [Ca2+]i and a reversal potential close to the K+ equilibrium potential, occurred if the membrane potential was clamped back to 0 mV. They were absent if intracellular K+ was replaced by Cs+ and blocked by extracellular tetraethylammonium (5 mM), Ba2+ (1 mM), or a membrane-permeable adenosine 3',5'-cyclic monophosphate analogue. These observations are discussed in relation to cell proliferation. The enhanced expression of K+ channels during cell proliferation provides a positive-feedback mechanism resulting in long-term changes in [Ca2+]i required for the G1-S transition in the cell cycle.

Potassium distribution and membrane potential of sensory neurons in the leech nervous system

1984 ◽  
Vol 51 (4) ◽  
pp. 689-704 ◽  
Author(s):  
W. R. Schlue ◽  
J. W. Deitmer
Keyword(s):  
Nervous System ◽  
Membrane Potential ◽  
Sensory Neurons ◽  
Membrane Resistance ◽  
Equilibrium Potential ◽  
Bathing Medium ◽  
Membrane Hyperpolarization ◽  
K Concentration ◽  
Intracellular K Activity ◽  
K Activity

The intracellular K activity (aKi) and membrane potential of sensory neurons in the leech central nervous system were measured in normal and altered external K+ concentrations, [K+]o, using double-barreled, liquid ion-exchanger microelectrodes. In control experiments membrane potential measurements were made using potassium chloride-filled single-barreled microelectrodes. All values are means +/- SD. At the normal [K+]o (4 mM) the mean aKi of all cells tested was 72.6 +/- 10.6 mM (n = 40) and the average membrane potential was -47.3 +/- 5.2 mM (n = 40). When measured with single-barreled microelectrodes, the membrane potential averaged -45.3 +/- 2.9 mV (n = 12). Assuming an intracellular K+ activity coefficient of 0.75, the intracellular K+ concentration of sensory neurons would be 96.8 +/- 14.1 mM). With an extracellular K+ concentration of 5.8 mM in the intact ganglion compared to the K+ concentration of 4 mM in the bath, the K+ equilibrium potential was -71.5 mV. When the ganglion capsule was opened, the extracellular K+ concentrations in the ganglion were similar to that of the bathing medium and the calculated K+ equilibrium potential was -81 mV. The membrane of sensory neurons depolarized following the changes to elevated [K+]o (greater than or equal to 10-100 mM), whereas aKi changed only little or not at all. At very low [K+]o (0.2, 0 mM) aKi and membrane potential showed little short-term (less than 3 min) effect but began to change after longer exposure (greater than 3 min). Reduction of [K+]o from 4 to 0.2 mM (or 0 mM) produced first a slow, and then a more rapid decrease of aKi and membrane resistance, accompanied by a slow membrane hyperpolarization. Following readdition of normal [K+]o, the membrane first depolarized and then transiently hyperpolarized, eventually returning slowly to the normal membrane potential.(ABSTRACT TRUNCATED AT 400 WORDS)

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.

Sign in / Sign up

Export Citation Format

Share Document