Frusemide-Sensitive Sodium and Potassium Transport by Human Leucocytes

1985 ◽  
Vol 68 (1) ◽  
pp. 89-91 ◽  
Author(s):  
Valerie E. Johnson ◽  
P. J. Hilton

1. Frusemide-sensitive sodium and potassium transport by normal human leucocytes has been studied in vitro by both isotopic and net flux techniques. 2. In physiological media the leucocyte exhibits a frusemide-sensitive influx of sodium and potassium of equal magnitude compatible with a 1:1 co-transport system. 3. Cells exposed to zero external sodium and potassium (osmolality maintained with choline) demonstrated a frusemide-sensitive sodium and potassium efflux. 4. Frusemide-sensitive potassium influx was dependent on the presence of external sodium but frusemide-sensitive sodium influx persisted unchanged in the absence of external potassium. 5. Frusemide-sensitive potassium influx was dependent on external chloride but frusemide-sensitive sodium influx was chloride-independent. 6. These last two observations make it likely that the frusemide-sensitive pathway is capable of operating in modes other than sodium-potassium co-transport.

1981 ◽  
Vol 61 (3) ◽  
pp. 307-312 ◽  
Author(s):  
R. B. Jones ◽  
J. Patrick ◽  
P. J. Hilton

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.


1974 ◽  
Vol 46 (5) ◽  
pp. 613-617 ◽  
Author(s):  
P. J. Hilton ◽  
J. Patrick

1. Sodium and potassium transport rates were studied in normal human leucocytes exposed to iso-osmolal and hypo-osmolal extracellular fluid. 2. Hypo-osmolality of the extracellular fluid led to an increase in sodium influx and a decrease in potassium influx expressed as mmol h−1 kg−1 cell dry weight. The fall in potassium influx was smaller than the rise in sodium influx and was confined to the ouabain-insensitive portion of the flux. 3. The rate constants for sodium and potassium efflux did not differ significantly between the iso-osmolal and hypo-osmolal media.


1975 ◽  
Vol 49 (5) ◽  
pp. 385-390
Author(s):  
P. J. Hilton ◽  
R. P. S. Edmondson ◽  
R. D. Thomas ◽  
J. Patrick

1. Sodium and potassium transport rates in human leucocytes were measured in vitro at different external potassium concentrations. 2. At nominally zero external potassium concentrations, the ouabain-sensitive sodium efflux was reduced to less than 20% of its maximum value. There was evidence that under these conditions a ouabain-sensitive sodium-sodium exchange occurs. 3. Both total and ouabain-insensitive potassium influx increased with increasing external potassium concentration. The ouabain-sensitive potassium influx showed saturation. 4. Ouabain-insensitive potassium efflux was also stimulated by increasing the external potassium concentration, suggesting significant potassium-potassium exchange at physiological external potassium concentrations.


1973 ◽  
Vol 44 (5) ◽  
pp. 439-445 ◽  
Author(s):  
P. J. Hilton ◽  
J. Patrick

1. Sodium and potassium efflux and influx rates were studied in normal human leucocytes in an artificial extracellular fluid using radioactive isotopes. 2. The rate constant for sodium efflux was 4.2 h−1 corresponding to a sodium efflux rate of 487 mmol kg cell dry weight−1 h−1. Approximately three-quarters of this flux was ouabain sensitive. 3. Potassium influx was 346 mmol kg cell dry weight−1 h−1. Approximately two-thirds of the potassium influx was ouabain insensitive.


1963 ◽  
Vol 47 (2) ◽  
pp. 379-392 ◽  
Author(s):  
H. Kimizuka ◽  
K. Koketsu

The changes in the membrane permeability to sodium, potassium, and chloride ions as well as the changes in the intracellular concentration of these ions were studied on frog sartorius muscles in Ca-free EDTA solution. It was found that the rate constants for potassium and chloride efflux became almost constant within 10 minutes in the absence of external calcium ions, that for potassium increasing to 1.5 to 2 times normal and that for chloride decreasing about one-half. The sodium influx in Ca-free EDTA solution, between 30 and 40 minutes, was about 4 times that in Ringer's solution. The intracellular sodium and potassium contents did not change appreciably but the intracellular chloride content had increased to about 4 times normal after 40 minutes. By applying the constant field theory to these results, it was concluded that (a) PCl did not change appreciably whereas PK decreased to a level that, in the interval between 10 and 40 minutes, was about one-half normal, (b) PNa increased until between 30 and 40 minutes it was about 8 times normal. The low value of the membrane potential between 30 and 40 minutes was explained in terms of the changes in the membrane permeability and the intracellular ion concentrations. The mechanism for membrane depolarization in this solution was briefly discussed.


1982 ◽  
Vol 94 (1) ◽  
pp. 99-NP ◽  
Author(s):  
S. Fenton ◽  
E. Clarkson ◽  
G. MacGregor ◽  
J. Alaghband-Zadeh ◽  
H. E. de Wardener

A highly sensitive cytochemical method for the assay of the ability of plasma and extracts of human urine to stimulate renal glucose-6-phosphate dehydrogenase (G6PD) activity in vitro is described. In the proximal convoluted tubules there was a linear increase of G6PD activity with the logarithm of concentration of a highly purified natriuretic extract from normal human urine (0·384–384 ng active material/l) which was used as a standard. The stimulation of G6PD obtained with dilutions of normal human plasma was parallel to that produced by the standard. The sensitivity of the assay permitted the measurement of as little as 0·384 ng active material/l of the natriuretic extract (0·001 units/ml) and dilutions of 1/10 000 could be detected using normal human plasma. The mean ± s.e.m. index of precision was 0·068± 0·003 (n = 9). It is known that inhibition of sodium potassium-dependent adenosine triphosphatase (Na+-K+-ATPase) is associated with a rise in G6PD activity. We have confirmed this observation by demonstrating that ouabain, a potent inhibitor of Na+ -K+-ATPase, stimulates renal G6PD activity in our assay and that natriuretic extract, human plasma and ouabain stimulated renal G6PD activity in vitro and simultaneously inhibited renal Na+-K+-ATPase activity in vitro. The plasma from 12 normal subjects (five of whom were previously shown to inhibit renal Na+-K+-ATPase activity in vitro in a manner related to sodium intake) stimulated renal G6PD activity in vitro, and this activity was also directly related to sodium intake. It is suggested that the change in the capacity of plasma to stimulate renal G6PD activity in vitro is a marker of the concentration of a circulating sodium transport inhibitor.


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