scholarly journals Strophanthidin-sensitive sodium fluxes in metabolically poisoned frog skeletal muscle.

1976 ◽  
Vol 68 (4) ◽  
pp. 405-420 ◽  
Author(s):  
B G Kennedy ◽  
P De Weer
Keyword(s):  
Skeletal Muscle ◽  
Membrane Potential ◽  
Human Erythrocyte ◽  
Sodium Pump ◽  
Giant Axon ◽  
Squid Giant Axon ◽  
Frog Skeletal Muscle ◽  
Na Efflux ◽  
Unidirectional Fluxes ◽  
External K

Strophanthidin-sensitive and insensitive unidirectional fluxes of Na were measured in fog sartorius muscles whose internal Na levels were elevated by overnight storage in the cold. ATP levels were lowered, and ADP levels raised, by metabolic poisoning with either 2,4-dinitrofluorobenzene or iodoacetamide. Strophanthidin-sensitive Na efflux and influx both increased after poisoning, while strophanthidin-insensitives fluxes did not. The increase in efflux did not require the presence of external K but was greatly attenuated when Li replaced Na as the major external cation. Membrane potential was not markedly altered by 2,4-dinitrofluorobenzene. These observations indicate that the sodium pump of frog skeletal muscle resembles that of squid giant axon and human erythrocyte in its ability to catalyze Na-Na exchange to an extent determined by intracellular ATP/ADP levels.

scholarly journals Sodium and potassium fluxes and membrane potential of human neutrophils: evidence for an electrogenic sodium pump.

1982 ◽  
Vol 79 (3) ◽  
pp. 453-479 ◽  
Author(s):  
L Simchowitz ◽  
I Spilberg ◽  
P De Weer
Keyword(s):  
Membrane Potential ◽  
Sodium Pump ◽  
Membrane Conductance ◽  
Human Neutrophils ◽  
Constant Field ◽  
Electrogenic Sodium Pump ◽  
Na Efflux ◽  
The Individual ◽  
Sodium And Potassium ◽  
External K

Sodium and potassium ion contents and fluxes of isolated resting human peripheral polymorphonuclear leukocytes were measured. In cells kept at 37 degrees C, [Na]i was 25 mM and [K]i was 120 mM; both ions were completely exchangeable with extracellular isotopes. One-way Na and K fluxes, measured with 22Na and 42K, were all approximately 0.9 meq/liter cell water . min. Ouabain had no effect on Na influx or K efflux, but inhibited 95 +/- 7% of Na efflux and 63% of K influx. Cells kept at 0 degree C gained sodium in exchange for potassium ([Na]i nearly tripled in 3 h); upon rewarming, ouabain-sensitive K influx into such cells was strongly enhanced. External K stimulated Na efflux (Km approximately 1.5 mM in 140-mM Na medium). The PNa/PK permeability ratio, estimated from ouabain insensitive fluxes, was 0.10. Valinomycin (1 microM) approximately doubled PK. Membrane potential (Vm) was estimated using the potentiometric indicator diS-C3(5); calibration was based on the assumption of constant-field behavior. External K, but not Cl, affected Vm. Ouabain caused a depolarization whose magnitude dependent on [Na]i. Sodium-depleted cells became hyperpolarized when exposed to the neutral exchange carrier monensin; this hyperpolarization was abolished by ouabain. We conclude that the sodium pump of human peripheral neutrophils is electrogenic, and that the size of the pump-induced hyperpolarization is consistent with the membrane conductance (3.7-4.0 microseconds/cm2) computed from the individual K and Na conductances.

Electric current generated by squid giant axon sodium pump: external K and internal ADP effects

1978 ◽  
Vol 235 (1) ◽  
pp. C63-C68 ◽  
Author(s):  
R. F. Abercrombie ◽  
P. de Weer
Keyword(s):  
Sodium Pump ◽  
Giant Axon ◽  
Pump Current ◽  
Membrane Resistance ◽  
Extracellular Potassium ◽  
Sodium Efflux ◽  
Steroid Sensitive ◽  
External Potassium ◽  
Loligo Pealei ◽  
External K

The operation of the sodium pump of giant axons of the squid, Loligo pealei, has been studied simultaneously in two independent ways: 1) by measuring sodium efflux with 22Na, and 2) by calculating the transmembrane current generated by the pump from measurements of membrane resistance and digitalis-sensitive membrane potential. In normal, untreated axons, the effect of increasing the external potassium concentration on both sodium efflux and pump current is similar, which suggests that Na:K pump stoichiometry remains relatively constant in the range of 0-20 mM external K. The data are compatible with a 3:2 Na:K ratio. In axons whose intracellular ADP level has been elevated by injection of L-arginine, a large, electrically silent, cardiotonic steroid-sensitive sodium efflux takes place in the absence of external potassium; this suggests that pump-mediated Na:Na exchange is 1:1 or electroneutral. Finally, elevation of external potassium levels causes the appearance, in high-ADP axons, of electrogenic pumping, with little effect on sodium efflux; hence, in contrast to what is seen in normal (low-ADP) axons, the charge translocated, per sodium ion extruded, increases sharply with increasing extracellular potassium levels.

Effects of pH changes on sodium pump fluxes in squid giant axon

1987 ◽  
Vol 253 (4) ◽  
pp. C547-C554 ◽  
Author(s):  
G. E. Breitwieser ◽  
A. A. Altamirano ◽  
J. M. Russell
Keyword(s):  
Sodium Pump ◽  
Maximum Velocity ◽  
Activation Parameters ◽  
Giant Axon ◽  
Inhibitory Effect ◽  
Squid Giant Axon ◽  
Extracellular Ph ◽  
Sodium Efflux ◽  
Effects Of Ph ◽  
Ph Range

The effects of independently varying intracellular and extracellular pH on sodium pump fluxes were studied in the squid giant axon. By means of intracellular dialysis, we found that changes of intracellular pH (pHi), but not of extracellular pH, affected ouabain-sensitive Na+ efflux and K+ influx over the pH range of 6.0-8.6. Both fluxes were maximum at a pHi of 7.2-7.4. Variations away from this optimal pHi in either the acidic or alkaline direction resulted in a graded inhibition of both ouabain-sensitive fluxes. The kinetic basis for the inhibitory effect of acidic pHi was examined by comparing the kinetic parameters of activation of ouabain-sensitive sodium efflux by intracellular Na+ (Na+i) and extracellular K+ (K+o) at normal pHi with those at acidic pHi. We found that the inhibitory effect of intracellular acidity results from a reversible decrease in maximum velocity (Vmax), without an effect on the activation parameters for Na+i (K1/2 Na+i) or K+o (K1/2 K+o).

scholarly journals Non-Linear Current-Potential Relations in an Axon Membrane

1961 ◽  
Vol 44 (6) ◽  
pp. 1055-1057 ◽  
Author(s):  
Kenneth S. Cole
Keyword(s):  
Membrane Potential ◽  
Giant Axon ◽  
Squid Giant Axon ◽  
External Current ◽  
Current Electrode ◽  
Axon Membrane ◽  
Linear Current ◽  
One Step ◽  
Original Derivation ◽  
Current Potential

The membrane current density, Im, in the squid giant axon has been calculated from the measured external current applied to the axon, Io, by the equation See PDF for Equation where Vm is the membrane potential under the current electrode and r1 and r2 are the external and internal longitudinal resistances. The original derivation of this equation included in one step an assumption of a linear relation between Im and Vm. It is shown that the same equation can be obtained without this restricting assumption.

scholarly journals The Influence of External Potassium on the Inactivation of Sodium Currents in the Giant Axon of the Squid, Loligo pealei

1969 ◽  
Vol 53 (6) ◽  
pp. 685-703 ◽  
Author(s):  
William J. Adelman ◽  
Yoram Palti
Keyword(s):  
Steady State ◽  
Membrane Potential ◽  
Membrane Conductance ◽  
Absolute Magnitude ◽  
Giant Axon ◽  
Membrane Potentials ◽  
Initial Transient ◽  
External Potassium ◽  
Loligo Pealei ◽  
External K

Isolated giant axons were voltage-clamped in seawater solutions having constant sodium concentrations of 230 mM and variable potassium concentrations of from zero to 210 mM. The inactivation of the initial transient membrane current normally carried by Na+ was studied by measuring the Hodgkin-Huxley h parameter as a function of time. It was found that h reaches a steady-state value within 30 msec in all solutions. The values of h∞, τh, αh,and ßh as functions of membrane potential were determined for various [Ko]. The steady-state values of the h parameter were found to be inversely related, while the time constant, τh, was directly related to external K+ concentration. While the absolute magnitude as well as the slopes of the h∞ vs. membrane potential curves were altered by varying external K+, only the magnitude and not the shape of the corresponding τh curves was altered. Values of the two rate constants, αh and ßh, were calculated from h∞ and τh values. αh is inversely related to [Ko] while ßh is directly related to [Ko] for hyperpolarizing membrane potentials and is independent of [Ko] for depolarizing membrane potentials. Hodgkin-Huxley equations relating αh and ßh to Em were rewritten so as to account for the observed effects of [Ko]. It is concluded that external potassium ions have an inactivating effect on the initial transient membrane conductance which cannot be explained solely on the basis of potassium membrane depolarization.

The diffusion and electrogenic components of the membrane potential of hypoxic myocardium

1987 ◽  
Vol 65 (2) ◽  
pp. 246-251 ◽  
Author(s):  
Normand Leblanc ◽  
Elena Ruiz-Ceretti
Keyword(s):  
Membrane Potential ◽  
Sodium Pump ◽  
Resting Potential ◽  
Krebs Solution ◽  
Ventricular Muscle ◽  
Diffusion Component ◽  
K Concentration ◽  
Zero Potential ◽  
K Permeability ◽  
External K

The diffusion and electrogenic components of the resting potential of hypoxic ventricular muscle were separated by inhibition of the sodium pump with 10−4 M ouabain. The response to varying external K concentrations (Ko) was studied. Arteriaily perfused rabbit hearts were submitted to 60 min hypoxia in Krebs solution containing 5 mM K throughout or to different external K concentrations during the last 20 min of hypoxia. For K concentrations between 1.5 and 10 mM, hypoxia did not change the resting potential except for a slight hyperpolarization in 7.5 mM K. The diffusion component of the resting potential did not differ from the resting potential at Ko < 5 mM. An electrogenic potential of −3 to −6 mV was detectable at Ko values between 5 and 10 mM. The internal K concentration, Ki, was estimated from extrapolations to zero potential of the relation resting potential vs. Ko in normoxic and hypoxic hearts. These experiments revealed a decline of Ki of 16 mM with hypoxia. The variation of the diffusion potential with external K was fitted by a PNa:PK ratio five times lower than in normoxia. It has been concluded that an increase in K permeability and the persistence of electrogenic Na extrusion during hypoxia of rather short duration prevent membrane depolarization despite the myocardial K loss.

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