Nombres de Transport, tK, tNa et tca Pour la Membrane de la Cellule Hépatique In Vivo

1972 ◽  
Vol 50 (5) ◽  
pp. 416-422 ◽  
Author(s):  
Jean Pierre Caillé ◽  
O. F. Schanne
Keyword(s):  
Membrane Potential ◽  
Liver Cell ◽  
Ionic Mobility ◽  
Irreversible Thermodynamics ◽  
Transport Numbers ◽  
Experimental Conditions ◽  
External Potassium ◽  
K Concentration ◽  
External K

We measured the membrane potential of the liver cell in vivo at 38 °C as we increased the external potassium. For the range of K concentration from 20.4 to 78 mM, the membrane potential of the liver cell decreased with a slope of 20.2 mV per decade change in external K concentration. The tissue content of K, Na, and Cl was analyzed under the same experimental conditions. The cytoplasmic resistivity (111 ± 17.5 Ω-cm) was used as a criterion for the state of the ions in the cytoplasm. This result, when it is compared with the value predicted from the ionic content, suggests that either the ionic mobility or the ionic activity in the cytoplasm of the liver cell is less than in a simple salt solution. An analytical expression, derived with the use of irreversible thermodynamics, permits us to calculate the transport numbers for the ions K, Na, and Cl in the membrane of the liver cell (tK 0.28, tNa 0.12, tCl 0.61).

Intracellular chloride activity in rabbit papillary muscle: effect of serum

1986 ◽  
Vol 64 (11) ◽  
pp. 1381-1384 ◽  
Author(s):  
Jean-Pierre Caillé
Keyword(s):  
Membrane Potential ◽  
Cardiac Cells ◽  
Equilibrium Potential ◽  
Papillary Muscles ◽  
Experimental Conditions ◽  
Intracellular Chloride ◽  
Intracellular Chloride Activity ◽  
Chloride Activity ◽  
Diastolic Potential

The intracellular chloride activity (aiCl), measured with Cl-selective microelectrodes on stimulated rabbit papillary muscles (1 Hz) incubated in serum, was 7.2 ± 2.2 mM (48 measurements). Under the same condition, on the quiescent muscle, aiCl was 7.5 ± 2.8 mM (45 measurements). The membrane potential of quiescent papillary muscles and diastolic potential of stimulated papillary muscles were −79.0 ± 0.7 (50 measurements) and −83.5 ± 0.5 mV (50 measurements), respectively. The experimental conditions were chosen to reproduce the in vivo conditions where the Cl equilibrium potential is close to the membrane potential or to the diastolic potential. After correcting for cytoplasmic interference (4 mM) on the aiCl measurements, the Cl equilibrium potential (ECl) was −84 mV. In conclusion, the Cl distribution in cardiac cells bathed in serum is passive as for in vivo cardiac cells.

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.

scholarly journals The influence of external cations and membrane potential on Ca-activated Na efflux in Myxicola giant axons.

1978 ◽  
Vol 71 (4) ◽  
pp. 453-466 ◽  
Author(s):  
R A Sjodin ◽  
R F Abercrombie
Keyword(s):  
Membrane Potential ◽  
Direct Action ◽  
Monovalent Cation ◽  
Coupling Ratio ◽  
Large Component ◽  
Experimental Conditions ◽  
Giant Axons ◽  
Threefold Increase ◽  
Na Efflux ◽  
External K

In microinjected Myxicola giant axons with elevated [Na]i, Na efflux was sensitive to Cao under some conditions. In Li seawater, sensitivity to Cao was high whereas in Na seawater, sensitivity to Cao was observed only upon elevation of [Ca]o above the normal value. In choline seawater, the sensitivity of Na efflux to Cao was less than that observed in Li seawater whereas Mg seawater failed to support any detectable Cao-sensitive Na efflux. Addition of Na to Li seawater was inhibitory to Cao-sensitive Na efflux, the extent of inhibition increasing with rising values of [Na]o. The presence of 20 mM K in Li seawater resulted in about a threefold increase in the Cao-activated Na efflux. Experiments in which the membrane potential, Vm, was varied or held constant when [K]o was changed showed that the augmentation of Ca-activated Na efflux by Ko was not due to changes in Vm but resulted from a direct action of K on activation by Ca. The same experimental conditions that favored a large component of Cao-activated Na efflux also caused a large increase in Ca influx. Measurements of Ca influx in the presence of 20 mM K and comparison with values of Ca-activated Na efflux suggest that the Na:Ca coupling ratio may be altered by increasing external [K]o. Overall, the results suggest that the Cao-activated Na efflux in Myxicola giant axons requires the presence of an external monovalent cation and that the order of effectiveness at a total monovalent cation concentration of 430 mM is K + Li greater than Li greater than Choline greater than Na.

scholarly journals Cat Heart Muscle in Vitro

1965 ◽  
Vol 48 (5) ◽  
pp. 933-948 ◽  
Author(s):  
Jon Goerke ◽  
Ernest Page
Keyword(s):  
Steady State ◽  
Membrane Potential ◽  
Papillary Muscle ◽  
Heart Muscle ◽  
Volume Ratio ◽  
K Concentration ◽  
Linear Manner ◽  
Cat Heart ◽  
External K

The exchange of cell K with K42, JK, has been measured in cat right ventricular papillary muscle under conditions of a steady state with respect to intracellular K concentration. Within the limits of the measurement, all of cell K exchanged at a single rate. Cells from small cats are smaller and have larger surface/volume ratios than cells from large cats. The larger surface/volume ratio results in larger flux values. JK increases in an approximately linear manner as the external K concentration is increased twentyfold, from 2.5 to 50 mM, at constant intracellular K concentration. The permeability for K ions, PK, calculated from the influx and membrane potential, remains very nearly constant over this range of external K concentrations. JK is not affected by replacement of O2 by N2, or by stimulated contractions at 60 per minute, but K influx decreases markedly in 10-5 M and 10-8 M ouabain.

scholarly journals The protonmotive potential difference across the vacuo-lysosomal membrane of Hevea brasiliensis (rubber tree) and its modification by a membrane-bound adenosine triphosphatase

1981 ◽  
Vol 198 (2) ◽  
pp. 365-372 ◽  
Author(s):  
B Marin ◽  
M Marin-Lanza ◽  
E Komor
Keyword(s):  
Membrane Potential ◽  
Hevea Brasiliensis ◽  
Ph Dependence ◽  
Rubber Tree ◽  
Lysosomal Membrane ◽  
Potential Difference ◽  
Experimental Conditions ◽  
Carbonyl Cyanide ◽  
Membrane Bound ◽  
K Concentration

The vacuo-lysosomes of Hevea brasiliensis (rubber tree) constitute a suitable model system for the study of active transport and energization at the level of the membrane of plant vacuoles. The pH gradient (delta pH) and the membrane potential (delta psi) of vacuo-lysosomes were determined by means of the weak base methylamine and the lipophilic cation tetraphenylphosphonium. The values obtained depended strongly on the experimental conditions such as medium pH or K+ concentration. Under experimental conditions, i.e., pH 7.5 outside and low K+, the delta pH amounts to about 0.9 unit, interior acid, and the delta psi to -120 mV, interior negative. The delta psi is presumably caused by the imposed K+ gradient, and the internal acidification might be a consequence of the passive proton inflow along the electric field. This explanation is sustained by the ineffectiveness of carbonyl cyanide p-trifluoromethoxyphenylhydrazone in destroying the delta pH and delta psi, whereas higher K+ concentration decreased both. Under conditions existing in vivo, the membrane potential might be significantly lower. The presence of ATP increased the acidification of the intravesicular space by 0.5pH unit to a delta pH of up to 1.4 and shifts the membrane potential at least 60mV to a more positive value. The change of the protonmotive potential did not occur with ADP; the pH-dependence of the change was identical with the pH-dependence of a vacuo-lysosomal membrane-bound ATPase, and the effect of ATPase was prevented by the presence of the uncoupler carbonyl cyanide p-trifluoromethoxyphenylhydrazone. The change of protonmotive potential difference, brought about by the ATPase, was at least 90 mV. This is evidence that a vacuo-lysosomal ATPase in plants can function as an electrogenic proton pump that transfers protons into the vacuo-lysosomal space.

Physiological effect of circulating glucagon on the hepatic membrane potential

2001 ◽  
Vol 281 (5) ◽  
pp. R1540-R1544
Author(s):  
Thomas A. Lutz ◽  
Alois Estermann ◽  
Nori Geary ◽  
Erwin Scharrer
Keyword(s):  
Membrane Potential ◽  
Cell Membrane ◽  
Liver Cell ◽  
Binding Capacity ◽  
Physiological Effect ◽  
Cell Membrane Potential ◽  
Male Rats ◽  
Liver Cell Membrane

The pancreatic hormone glucagon hyperpolarizes the liver cell membrane under various conditions. Here we investigated the physiological relevance of this effect by testing the influence of infusions of glucagon antiserum on the liver cell membrane potential in vivo. Intracellular microelectrode recordings of liver cells (up to 60/rat over 2 h) were done in anesthetized male rats. Livers were fixed in place, and recordings were done 10–30 min after intraperitoneal injections of glucagon or hepatic portal vein infusions of glucagon or specific polyclonal glucagon antibodies raised in rabbits. The isotonic lactose vehicle was used as a control for glucagon, and equal amounts of nonimmunized rabbit IgG were used as a control for glucagon antibodies. Intraperitoneal glucagon (400 μg/kg) hyperpolarized the liver cell membrane up to 12 mV, and intraportal glucagon (10 or 60 μg/kg) dose dependently hyperpolarized the liver cell membrane by 3–7 mV. Intraportal infusion of glucagon antiserum (in vitro binding capacity of 4 ng glucagon/rat) significantly depolarized the liver cell membrane by ∼2.5 mV. The effects of both glucagon and glucagon antiserum reversed after 60–90 min. We conclude that glucagon is a physiologically important modulator of the liver cell membrane potential.

In vivo and in vitro miniature end-plate potentials at various external K concentrations

1975 ◽  
Vol 228 (6) ◽  
pp. 1733-1737 ◽  
Author(s):  
S Muchnik ◽  
BA Kotsias ◽  
EE Arrizurieta de Muchnik
Keyword(s):  
Water Distribution ◽  
Ionic Composition ◽  
Synaptic Activity ◽  
Extracellular Potassium ◽  
Experimental Conditions ◽  
End Plate ◽  
External Potassium ◽  
Potassium Loading

In order to obtain a nore reliable picture of transmitter release, spontaneous synaptic activity was studied in vivo in the rat soleus neuromuscular junction. The in vivo miniature end-plate potential (MEPP) recordings were compared with those obtained in vitro and, in both circumstances, MEPP frequency was measured at external potassiumconcentrations ranging from 5 to 15 mM. The influence of external potassium loading on intra- and extracellular potassium concentration also estimated by measuring the muscle ionic composition and water distribution at normal and high plasma potassium concentrations. The MEPP frequencies recorded in vivo were consistently lower than those observed in vitro for all external potassium concentrations studied (P less than0.01). These data suggest that better experimental conditions are maintained in thein vivo preparations, since the intracellular potassium increase that follows the external potassium loading can only partially justify the observed differnce and other factors, such as anesthetic effects, etc, may be ruled out.

Potassium loss from hypoxic myocardium: influence of external K concentration

1987 ◽  
Vol 65 (5) ◽  
pp. 861-866 ◽  
Author(s):  
Normand Leblanc ◽  
Elena Ruiz-Ceretti ◽  
Denis Chartier
Keyword(s):  
Electrical Activity ◽  
Sodium Content ◽  
Total Water ◽  
Tissue Samples ◽  
Normal Medium ◽  
High K ◽  
Voltage Dependent ◽  
External Potassium ◽  
K Concentration ◽  
External K

The influence of external potassium Ko and tetraethylammonium on the cellular K content of hypoxic myocardium was investigated. Perfused rabbit hearts were submitted to 60 min hypoxia in medium containing 5 mM K throughout or either low (1.5 mM) or high (10 mM) K during the last 20 min of hypoxia. Paced electrical activity (2.5 Hz) was kept throughout the experiments. Tissue samples excised from the left ventricle were analyzed for total water, inulin space, and Na and K content. Lowering Ko to 1.5 mM increased both K loss and Na accumulation. Addition of 3.5 mM RbCl under these conditions reversed Na accumulation to levels found for hypoxia in normal medium but did not modify the cellular K loss. Tetraethylammonium (10 mM) did not alter Na accumulation but partly prevented the decrease in K content produced by hypoxia. A similar effect was observed by increasing Ko to 10 mM. At this high Ko prolongation of hypoxia did not enhance K loss. Abolition of electrical activity by TTX in a high K solution prevented K loss and reduced the sodium content. These results are consistent with the view that voltage-dependent channels are implicated in the K loss induced by hypoxia or ischemia. Furthermore, they indicate that the K loss may be modulated by external K because of the influence of the electrochemical gradient on passive K efflux and thus provide an explanation for the existence of a plateau in the early extracellular K accumulation observed during cardiac ischemia.

scholarly journals THE EFFECT OF ACTH AND ADRENAL STEROIDS ON K TRANSPORT IN HUMAN ERYTHROCYTES

1954 ◽  
Vol 37 (5) ◽  
pp. 643-661 ◽  
Author(s):  
D. H. P. Streeten ◽  
A. K. Solomon
Keyword(s):  
Human Erythrocytes ◽  
Adrenal Steroids ◽  
Method Of Calculation ◽  
Normal Human ◽  
K Concentration ◽  
The Relationship ◽  
K Transport ◽  
External K

The effect of ACTH and adrenal steroids on K transport in human erythrocytes has been studied. A new method of calculation has revealed that in normal human erythrocytes the K transport is not independent of external K concentration as had previously been thought. The equation describing the relationship is, K influx (m.eq./liter cells hour) = [K]pi/(0.697 + 0.329 [K]pi) in which [K]pi refers to the plasma K concentration at the beginning of the experiment. At the physiological plasma K concentration of 4.65 m.eq./liter, K influx is 2.09 m.eq./liter cells hour; K efflux is 1.95 m.eq./liter cells hour and is independent of plasma K concentration. The effect of the infusion of ACTH and adrenal steroids on the K content of the erythrocytes was also studied. Infusions of ACTH or cortisone do not cause the expected loss in erythrocyte K content and may well cause a gain. Infusions of ACTH and cortisone decrease the rate of K influx and efflux slightly at all stages of the infusion, as measured in vitro in blood samples drawn at various times during and following the infusion. However, the erythrocytes incubated in vitro do not exhibit the same changes in K content as are found in vivo. Hydrocortisone added to normal cells in vitro also decreases both influx and efflux of K, without affecting the K content of the cells.

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