scholarly journals POTASSIUM UPTAKE BY THE DOG ERYTHROCYTE

1954 ◽  
Vol 37 (5) ◽  
pp. 631-641 ◽  
Author(s):  
Howard S. Frazier ◽  
Arthur Sicular ◽  
A. K. Solomon
Keyword(s):  
Activation Energy ◽  
Apparent Activation Energy ◽  
Potassium Concentration ◽  
Glucose Consumption ◽  
Extracellular Potassium ◽  
Physiological Concentration ◽  
Extracellular Potassium Concentration ◽  
External Potassium ◽  
Potassium Influx ◽  
K Concentration

The inward transport of potassium by separated dog erythrocytes has been studied at concentrations of potassium in the medium from 2.9 to 25.0 m.eq./liter and at 38.0 and 33.0°C. At the physiological concentration of external potassium (4.06 m.eq./liter medium), the inward potassium flux is 0.11 m.eq./liter cells hour and the glucose consumption is 2.0 mM/liter cells hour. The dependence of potassium influx on extracellular potassium concentration is given by the following equation, K influx (m.eq./liter cells hour) = 0.028 [K]amb. – 0.003 in which [K]amb. refers to the potassium concentration in the medium. In a single 93 hour experiment, 94 per cent of the intracellular potassium was exchanged at an apparently uniform rate. The average apparent activation energy for the process is 7,750 calories ± 2,000 calories/mol and there is some indication that the apparent activation energy of inward K transport decreases with increasing external K concentration.

Effect of Extracellular Potassium on the Transport of Sodium and Potassium in Rat Thymocytes

1981 ◽  
Vol 61 (3) ◽  
pp. 307-312 ◽  
Author(s):  
R. B. Jones ◽  
J. Patrick ◽  
P. J. Hilton
Keyword(s):  
Potassium Concentration ◽  
Extracellular Potassium ◽  
Sodium Influx ◽  
Potassium Efflux ◽  
Sodium Efflux ◽  
Extracellular Potassium Concentration ◽  
External Potassium ◽  
Potassium Influx ◽  
Sodium And Potassium

1. The effect of extracellular potassium on the transport of sodium and potassium in rat thymocytes has been studied in vitro. 2. A significant increase in the rate constant for total and ouabain-sensitive sodium efflux was demonstrated at an extracellular potassium concentration of 1 mmol/l as compared with that at either 0 or 2 mmol/l. 3. At potassium concentrations below 3 mmol/l ouabain-sensitive sodium influx was observed suggesting sodium-sodium exchange catalysed by the sodium pump. 4. Both total and ouabain-insensitive potassium efflux rose with external potassium. A small ouabain-sensitive potassium efflux was observed at all levels of external potassium studied. 5. Total and ouabain-insensitive potassium influx increased with external potassium, but did not appear to saturate. Ouabain-sensitive potassium influx reached a maximum at an external potassium concentration of 2 mmol/l then decreased with increasing external potassium.

Kidney epithelial cell growth is stimulated by lowering extracellular potassium concentration

1983 ◽  
Vol 244 (5) ◽  
pp. C429-C432 ◽  
Author(s):  
M. M. Walsh-Reitz ◽  
F. G. Toback
Keyword(s):  
Epithelial Cells ◽  
Potassium Concentration ◽  
Extracellular Fluid ◽  
Renal Tissue ◽  
Extracellular Potassium ◽  
Extracellular Potassium Concentration ◽  
Kidney Growth ◽  
Kidney Epithelial Cell ◽  
K Concentration ◽  
Low K

The factors that induce kidney growth in K+-depleted animals are unknown. To determine if the low extracellular fluid K+ concentration could act as a growth stimulus, cultures of monkey kidney epithelial cells from the BSC-1 line were studied in media with a low-K+ concentration. Growth of confluent cultures was accelerated maximally at a K+ concentration of 3.2 mM, whereas concentrations of 2.9 and 3.5 mM were also stimulatory but to a lesser extent. Because growing renal tissue from K+-depleted rats was previously found to exhibit increased uptake of nutrient molecules, evidence for enhanced uptake was sought in BSC-1 cells after exposure to low-K+ medium. The uptake of 10 different nutrient molecules was enhanced in cells exposed to low-K+ medium for 30 s. These observations indicate that a reduced extracellular K+ concentration per se stimulates proliferation of renal epithelial cells in culture and could be one of the factors that mediate kidney growth in K+-depleted animals.

Arachidonic-acid-activated membrane conductances in dissociated cardiac parasympathetic neurons from Necturus

1995 ◽  
Vol 74 (4) ◽  
pp. 1621-1627 ◽  
Author(s):  
J. M. Mulvaney ◽  
R. L. Parsons
Keyword(s):  
Arachidonic Acid ◽  
Potassium Current ◽  
Potassium Concentration ◽  
Reversal Potential ◽  
Extracellular Potassium ◽  
Induced Current ◽  
Extracellular Potassium Concentration ◽  
Parasympathetic Neurons ◽  
External Potassium ◽  
Inwardly Rectifying

1. Characteristics of the membrane currents activated by arachidonic acid (AA) in dissociated mudpuppy parasympathetic neurons have been determined using the perforated-patch whole cell recording technique. 2. In a sodium-containing physiological solution with 12.5 mM potassium, AA (10-50 microM) increased total membrane current produced by either depolarizing or hyperpolarizing voltage steps delivered from a holding potential of -40 mV. Decreasing the external potassium concentration from 12.5 to 2.5 mM shifted the reversal potential of the AA-induced current by 10 mV rather than the approximately 42 mV predicted for a highly potassium-selective channel. 3. In cells kept in sodium solution plus 12.5 mM potassium and treated with 20 microM nordihydroguaiaretic acid (NDGA), an inhibitor of the lipoxygenase pathway of AA metabolism, AA activated only inward currents following hyperpolarizing voltage steps. In this condition, the shift in reversal potential of the AA-induced current was 40 mV when extracellular potassium concentration was changed fivefold. Consequently, in cells treated with NDGA, AA appeared to activate only an inwardly rectifying potassium current. 4. Decreasing the extracellular chloride concentration by approximately 90% did not alter the reversal potential of the AA-activated current when the extracellular sodium concentration was kept constant and the external potassium concentration was 2.5 mM. In the low-chloride solution, AA potentiated both inward and outward current amplitudes. These results suggested that AA did not activate a chloride current in these cells. 5. In a sodium-deficient, N-methyl-D-glucamine (NMG)-containing solution, AA only activated currents for voltage steps to potentials more negative than the holding potential. In the NMG-substituted solution, changing the extracellular potassium concentration fivefold shifted the reversal potential of the AA-induced current by 40 mV. Therefore, in the NMG solution, AA primarily activated an inwardly rectifying potassium current. 6. Exchanging the control solution containing AA to an external solution containing AA and barium (barium blocks the inwardly rectifying potassium current) shifted the current-voltage relationship to more positive voltages such that the extrapolated reversal potential was approximately 0 mV. In other experiments, using the barium-containing solution, the reversal potential for the AA-induced current was -3.3 +/- 2.4 (SE) mV. 7. In conclusion, the results of the present study indicate that at least two membrane currents are activated in the presence of AA: an inwardly rectifying potassium current and an NDGA-sensitive, sodium-dependent current that has a reversal potential more positive than the potassium equilibrium potential. We suggest the second current component is due to the activation of a nonselective cationic conductance.

Extracellular potassium concentration in chronic alumina cream foci of cats

1984 ◽  
Vol 52 (3) ◽  
pp. 421-434 ◽  
Author(s):  
U. Heinemann ◽  
I. Dietzel
Keyword(s):  
Border Zone ◽  
Constant Current ◽  
Extracellular Potassium ◽  
Local Concentration ◽  
Base Line ◽  
Extracellular Potassium Concentration ◽  
Concentration Changes ◽  
K Concentration ◽  
Repetitive Electrical Stimulation ◽  
Normal Cortex

Changes in extracellular K+ concentration [( K+]o) were measured with ion-selective microelectrodes in chronic epileptic foci induced by topical application of A1(OH)3 cream on the sensorimotor cortex of cats. The foci were morphologically characterized by a scar surrounded by an area of marked gliosis. Base-line levels of [K+]o in gliotic tissue and its immediate border zone were comparable to those in normal cortical tissue. Peak levels of [K+]o obtained during repetitive electrical stimulation of the cortical surface and thalamic ventrobasal complex were only slightly enhanced with 11.6 mM in chronic foci and 10.8 mM in normal cortex. Iontophoretic K+ application into gliotic tissue was accompanied by slow negative potential shifts comparable to those observed in normal cortex. Passage of constant current through gliotic tissue caused local [K+]o changes in the vicinity of the current-passing electrode. Since these [K+]o changes were similar to those observed in normal tissue, it was concluded that the amount of transcellularly transported K ions was comparable in both tissues. Changes in the size of extracellular space (ES) were investigated by measuring local concentration changes of iontophoretically injected tetramethylammonium and choline ions. During stimulus-induced seizure activity, the ES shrank outside the gliotic area at sites of maximal [K+]o elevation, while it increased at sites within the gliotic tissue where [K+]o rises were smaller. The results suggest that the spatial buffer capacity of gliotic tissue for K+ is not severely impaired. Since the relationship between rises in [K+]o and subsequent undershoots at sites immediately bordering the gliotic tissue is comparable to that in normal cortex, the ability of this epileptic tissue for active K+ uptake appears to be unaffected. This conclusion is further supported by the observation that iontophoretically induced rises in [K+]o during undershoots are reduced to a similar extent as in normal cortex.

Disorders of potassium homeostasis

2010 ◽  
pp. 3831-3845 ◽  
Author(s):  
J Firth
Keyword(s):  
Membrane Potential ◽  
Potassium Concentration ◽  
Resting Membrane Potential ◽  
Extracellular Potassium ◽  
Normal Range ◽  
Critical Determinant ◽  
Potassium Homeostasis ◽  
Extracellular Potassium Concentration

The normal range of potassium concentration in serum is 3.5 to 5.0 mmol/litre and within cells it is 150 to 160 mmol/litre, the ratio of intracellular to extracellular potassium concentration being a critical determinant of cellular resting membrane potential and thereby of the function of excitable tissues....

Theoretical analysis of parameters leading to frequency modulation along an inhomogeneous axon

1976 ◽  
Vol 39 (4) ◽  
pp. 909-923 ◽  
Author(s):  
I. Parnas ◽  
S. Hochstein ◽  
H. Parnas
Keyword(s):  
Potassium Concentration ◽  
Single Step ◽  
Repetitive Firing ◽  
Extracellular Potassium ◽  
Pass Filter ◽  
Low Pass Filter ◽  
Extracellular Potassium Concentration ◽  
Spike Shape ◽  
Single Spike ◽  
Low Pass

1. Theoretical computations were conducted on a computer model of a segmented, nonhomogeneous axon to understand the mechanism of frequency block of conduction. 2. The model is based on the Hodgkin-Huxley equations modified in several ways to better describe the cockroach axon. We used cockroach parameters where available. 3. The increase in fiber radius was spread over a series of segments to approximate a taper. We found that a taper allows a larger overall increase in fiber diameter than a single step to be successfully passed. 4. We studied effects on a train of impulses. The modified equations included effects due to changes in extracellular potassium concentration resulting from the repetitive firing of the axon. 5. An increase in diameter which allows a single spike to pass blocks the subsequent impulses in a train at the taper if potassium concentration variability is introduced. This could explain the low-pass filter characteristics of axon constrictions. 6. Results of the model fit well with the experiemental spike shape and height. Data were computed for the refractory period and its dependence on the taper parameters.

Sodium dependence of carnitine transport in isolated perfused adult rat hearts

1983 ◽  
Vol 244 (2) ◽  
pp. H247-H252 ◽  
Author(s):  
T. C. Vary ◽  
J. R. Neely
Keyword(s):  
Potassium Concentration ◽  
Sodium Concentration ◽  
Extracellular Potassium ◽  
Extracellular Potassium Concentration ◽  
Rat Hearts ◽  
Carrier Mediated Transport ◽  
Physiological Serum ◽  
Carnitine Transport ◽  
Extracellular Sodium ◽  
Carnitine Concentration

In heart muscle, the intracellular carnitine concentration is approximately 40 times higher than the plasma carnitine concentration, suggesting the existence of an active transport process. At physiological serum carnitine concentrations (44 microM), 80% of total myocardial carnitine uptake occurs via a carrier-mediated transport system. The mechanism of this carrier-mediated transport was studied in isolated perfused rat hearts. Carnitine transport showed an absolute dependence on the extracellular sodium concentration. The rate of carnitine transport was linearly related to the perfusate sodium concentration at every perfusate carnitine concentration examined (15-100 microM). Total removal of extracellular sodium completely abolished the carrier-mediated transport. Decreasing the perfusate potassium concentration from a control of 5.9 to 0.6 mM stimulated transport by 35%, whereas increasing the extracellular potassium concentration from 5.9 to 25 mM reduced transport by 60%. The carrier-mediated transport was inversely proportional to the extracellular potassium concentration. Acetylcholine (10(-3) M), isoproterenol (10(-7) M), or ouabain (10(-3) did not alter the rate of carnitine transport. Addition of tetrodotoxin (10(-5) stimulated carnitine transport by about 40%, while gramicidin S (5 X 10(-6) M) decreased uptake by about 18% relative to control. The data provide evidence that carnitine transport by cardiac cells occurs by a Na+-dependent cotransport mechanism that is dependent on the Na+ electrochemical gradient.

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