Leucocyte Electrolytes and Sodium Efflux Rate Constants in the Hypertension of Pre-Eclampsia

1980 ◽  
Vol 59 (s6) ◽  
pp. 199s-201s ◽  
Author(s):  
T. E. Forrester ◽  
G. A. O. Alleyne
Keyword(s):  
Blood Pressure ◽  
Rate Constant ◽  
Rate Constants ◽  
Sodium Pump ◽  
Efflux Rate ◽  
Sodium Efflux ◽  
Pump Activity

1. Leucocyte electrolytes were measured in pre-eclampsia and comparison was made with leucocytes from normal primigravidae and from the original pre-eclamptic subjects 6 months after delivery when blood pressure had returned to normal. 2. In pre-eclamptic subjects, leucocyte sodium was elevated and potassium depressed, and the rate constant for sodium efflux was depressed. 3. These changes returned to normal after delivery. 4. An increase in cellular sodium as a result of altered sodium pump activity may be the cause of hypertension in pre-eclampsia.

Effect of the Calcium Antagonist Verapamil on Human Leucocyte Sodium Transport in vitro

1985 ◽  
Vol 68 (2) ◽  
pp. 239-241 ◽  
Author(s):  
H. H. Gray ◽  
L. Poston ◽  
V. E. Johnson ◽  
P. J. Hilton
Keyword(s):  
Essential Hypertension ◽  
Calcium Antagonist ◽  
Sodium Transport ◽  
Rate Constants ◽  
Sodium Pump ◽  
Efflux Rate ◽  
Sodium Efflux ◽  
Pump Activity ◽  
External Calcium

1. Sodium efflux rate constants and intracellular sodium were measured in leucocytes from healthy volunteers in the presence and absence of the calcium antagonist verapamil hydrochloride. 2. Verapamil stimulated sodium pump activity and this effect was dependent on the presence of external calcium. 3. Verapamil has been reported to reverse the abnormality of sodium transport seen in leucocytes from patients with essential hypertension and the present study demonstrates that sodium pump activity in leucocytes from control subjects is also stimulated by exposure to verapamil in vitro. This direct cellular effect appears to be due to the calcium antagonist properties of the drug.

Non-esterified fatty acids may regulate human leucocyte sodium pump activity

1986 ◽  
Vol 71 (6) ◽  
pp. 737-742 ◽  
Author(s):  
L. L. Ng ◽  
T. D. R. Hockaday
Keyword(s):  
Fatty Acids ◽  
Rate Constant ◽  
Acid Level ◽  
Sodium Pump ◽  
Efflux Rate ◽  
Fatty Acid Level ◽  
Esterified Fatty Acids ◽  
Pump Activity ◽  
Efflux Rate Constant

1. Human leucocyte sodium pump activity was studied in normal fasting subjects by measuring the ouabain-sensitive 22Na+ efflux rate constants. 2. This 22Na+ efflux rate constant was inversely related to the fasting plasma non-esterified fatty acid level (rs = −0.73, P < 0.0001). 3. An oral glucose load (40 g/m2 surface area) led to an increase in the leucocyte ouabain-sensitive 22Na+ efflux rate constant after 2 h (1.97 ± 0.25 to 2.44 ± 0.19 h−1, P < 0.0001, n = 11). There was a concomitant fall in the plasma non-esterified fatty acid level. 4. Incubation of leucocytes in vitro with 100 μmol/l linoleic acid inhibited the leucocyte ouabain-sensitive 22Na+ efflux rate constant (1.52 ± 0.27 vs 0.84 ± 0.24 h−1, P < 0.001, n = 8). 5. The leucocyte Na+,K+-dependent adenosine triphosphatase (Na+,K+-ATPase) activity was inhibited in vitro by long chain non-esterified fatty acids, especially when unsaturated. 6. Non-esterified fatty acids may account for some of the Na+,K+-ATPase inhibitory activity of plasma.

Erythrocyte 22Na Efflux and Urinary Sodium Excretion in Essential Hypertension

1980 ◽  
Vol 59 (s6) ◽  
pp. 195s-197s ◽  
Author(s):  
W. R. Fitzgibbon ◽  
T. O. Morgan ◽  
J. B. Myers
Keyword(s):  
Rate Constant ◽  
Sodium Excretion ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Aetiological Factor ◽  
Efflux Rate ◽  
Artificial Medium ◽  
Sodium Efflux ◽  
Hypertensive Patients ◽  
Efflux Rate Constant

1. The rate constant for total 22Na efflux from erythrocytes was examined in patients with mild to moderate hypertension and in normotensive controls. No difference in 22Na efflux rate constant was found when the cells from both groups were incubated in artificial medium. When the cells from both groups were incubated in their own plasma, the rate constant for Na efflux was significantly elevated for hypertensive patients compared with controls (0.40 ± 0.02, 0.36 ± 0.01 respectively; P&lt;0.05). 2. In hypertensive patients sodium efflux rate constant varied inversely with 24 h urinary sodium excretion when erythrocytes were incubated in artificial medium (r = − 0.34, P&lt;0.05) or in plasma (r = −0.42, P&lt;0.05). No association between sodium efflux rate constant and urinary sodium excretion occurred in normotensive subjects. 3. These findings provide further evidence that sodium is an important aetiological factor in hypertension. In ‘salt-sensitive’ individuals dietary sodium may interact with the regulation of cellular sodium transport via both humoral and cellular mechanisms to elevate blood pressure.

A comparison of endogenous digoxin-like immunoreactivity and sodium transport inhibitory activity in umbilical arterial and venous serum

1988 ◽  
Vol 75 (6) ◽  
pp. 577-579 ◽  
Author(s):  
J. F. Morris ◽  
L. Poston ◽  
C. D. Wolfe ◽  
P. J. Hilton
Keyword(s):  
Umbilical Cord ◽  
Rate Constant ◽  
Sodium Transport ◽  
Inhibitory Activity ◽  
Efflux Rate ◽  
Sodium Efflux ◽  
Cord Serum ◽  
Paired Samples ◽  
Efflux Rate Constant

1. Endogenous digoxin-like immunoreactivity (EDLI) was measured by radioimmunoassay for digoxin in 13 paired samples of arterial and venous umbilical cord serum. EDLI was present in vein and artery, but was higher in the venous samples (P < 0.025). 2. The venous cord serum inhibited the ouabain-sensitive sodium efflux rate constant of a normal mixed leucocyte population when compared with the effect of arterial cord serum (P < 0.005). 3. It is suggested that the placenta may be involved in the production or metabolism of neonatal EDLI and of the inhibitor of sodium transport.

Observations on the Measurement and Regulation of the Sodium Content of Rabbit Erythrocytes: Evidence for a Single Sodium Pump

1972 ◽  
Vol 50 (8) ◽  
pp. 791-797 ◽  
Author(s):  
E. K. M. Smith ◽  
D. Farrington ◽  
L. Sydiuk
Keyword(s):  
Rate Constant ◽  
Sodium Pump ◽  
Ethacrynic Acid ◽  
Sodium Content ◽  
Red Cells ◽  
Red Cell ◽  
Sodium Efflux ◽  
A Value ◽  
Active Transport Mechanism ◽  
Sodium Dependent

We have studied the cation content of rabbit erythrocytes; for a group of 40 animals red cell sodium was 9.2 ± 2.7 (S.D.) mmol/1 of cells, while potassium was 112 ± 8.6 mmol/1. Cell sodium content rose as the animals aged, but there was always a wide concentration gradient across the cell wall. This gradient was maintained by an active sodium pump, inhibited by ouabain (10−4 M) and comparable to pump I in the human red cell. The rate constant for this process in 16 rabbits was 0.313 ± 0.07 (S.D.) h−1, a value similar to that seen in man. Ethacrynic acid (10−3 M) inhibited a further component of sodium efflux, the rate constant being 0.259 ± 0.015 (S.D.) h−1. This was superficially comparable to pump II as previously described in the human; on further study, however, it was found to be sodium dependent, but able to function in the absence of adenosine triphosphate and incapable of net up-hill transport. These findings indicate that there is only one active transport mechanism in the red cells of the rabbit, which is a useful model for study in comparison to the red cells of man.

A Passive Sodium Transport Inhibitory Factor (Inhibitin) Released from Leukaemic Promyelocytes in Culture

1984 ◽  
Vol 66 (3) ◽  
pp. 365-368
Author(s):  
Kevin Morgan ◽  
M. Afzal Mir
Keyword(s):  
Rate Constant ◽  
Sodium Transport ◽  
Culture Media ◽  
Inhibitory Effect ◽  
Inhibitory Factor ◽  
Efflux Rate ◽  
Sodium Efflux ◽  
Stable Factor ◽  
Heat Stable ◽  
Efflux Rate Constant

1. Previous studies have shown that myeloid leukaemic blast cells contain a heat stable factor which inhibits bidirectional sodium transport in normal erythrocytes. This study was undertaken to establish whether leukaemic promyelocytes in culture secrete this factor. 2. Two cell-lines of leukaemic promyelocytes (HL-60 and JR) were grown and culture media from both reduced significantly the ouabain-insensitive sodium efflux rate constant, whereas conditioned culture medium (incubated like the cells in culture) had no inhibitory effect. 3. Promyelocyte extract reduced significantly (P < 0.01) the total sodium efflux rate constant from 0.393 ± 0.030 (sd) to 0.311 ± 0.060, and ouabain-insensitive efflux rate constant from 0.131 ± 0.008 to 0.079 ± 0.009 (P<0.001). 4. The inhibitory factor was heat stable (80°C for 30 min) and it inhibited sodium efflux through a pathway which was not inhibited by ouabain or frusemide. 5. These studies suggest that leukaemic promyelocytes secrete the previously identified passive sodium transport inhibitory factor.

A Study In Vitro of the Sodium Pump in Fulminant Hepatic Failure

1978 ◽  
Vol 55 (4) ◽  
pp. 355-363 ◽  
Author(s):  
A. N. Alam ◽  
Lucilla Poston ◽  
S. P. Wilkinson ◽  
C. G. Golindano ◽  
R. Williams
Keyword(s):  
Fulminant Hepatic Failure ◽  
Hepatic Failure ◽  
Sodium Pump ◽  
Normal Subjects ◽  
Sodium Content ◽  
Atp Content ◽  
Efflux Rate ◽  
Sodium Efflux ◽  
Reduced Activity

1. The mechanism underlying the raised leucocyte sodium content in fulminant hepatic failure was studied by measurement of sodium fluxes, (Na+ + K+)-dependent adenosine triphosphatase activity, and leucocyte ATP content. 2. The rate constant for sodium efflux in the leucocytes was significantly reduced, and attributable to reduced activity of the enzyme (Na+ + K+)-ATPase. Leucocyte ATP content was not significantly different from that of control cells. 3. Incubation of cells from patients in the sera of normal subjects resulted in a reversal of these changes. Inhibition of the leucocyte sodium efflux rate constants and (Na+ + K+)-ATPase of normal cells was achieved by incubation in sera from patients. 4. We suggest that the raised sodium content of leucocytes in fulminant hepatic failure is attributable to a defective sodium pumping mechanism, possibly due to a circulating toxin.

Effect of Hypokalaemia on the Ouabain-Sensitive Sodium Transport and the Ouabain-Binding Capacity in Human Erythrocytes

1983 ◽  
Vol 64 (2) ◽  
pp. 177-182 ◽  
Author(s):  
E. Jill Rubython ◽  
D. B. Morgan
Keyword(s):  
Rate Constant ◽  
Binding Capacity ◽  
Plasma Potassium ◽  
Inhibitory Effect ◽  
Sodium Content ◽  
Efflux Rate ◽  
Ouabain Binding ◽  
Sodium Efflux ◽  
Sodium Pumps ◽  
Efflux Rate Constant

1. The sodium content, the ouabain-sensitive sodium efflux and efflux rate constant and the ouabain-binding capacity were measured in the erythrocytes of 53 patients with hypokalaemia and in 37 healthy controls. The sodium content alone was measured in a further 57 patients with hypokalaemia. 2. In the patients with hypokalaemia there was an increase in the average sodium content of the erythrocytes, which was entirely due to a reduction in the ouabain-sensitive efflux rate constant. 3. The ratio of the ouabain-sensitive efflux rate constant to the number of sodium pumps was decreased in the patients with hypokalaemia, and was directly related to the plasma potassium. 4. Many patients with moderate hypokalaemia had normal erythrocyte sodium and potassium contents and normal ouabain-sensitive efflux rate constant. These patients had an increased number of sodium pumps, which compensated for the inhibitory effect of hypokalaemia on each sodium pump. 5. This increase in the number of sodium pumps was common even in patients who had probably had hypokalaemia for less than 2 weeks. This finding suggests that there are latent sodium pumps within the circulating erythrocytes.

The Relation between Membrane Cholesterol and Phospholipid and Sodium Efflux in Erythrocytes from Healthy Subjects and Patients with Chronic Cholestasis

1982 ◽  
Vol 62 (1) ◽  
pp. 101-107 ◽  
Author(s):  
P. A. Jackson ◽  
D. B. Morgan
Keyword(s):  
Rate Constant ◽  
Healthy Subjects ◽  
Sodium Content ◽  
Molar Ratio ◽  
Phospholipid Content ◽  
Efflux Rate ◽  
Sodium Efflux ◽  
Chronic Cholestasis ◽  
Efflux Rate Constant ◽  
Erythrocyte Sodium

1. The cholesterol and phospholipid content of the cell membrane and the efflux of sodium were measured in the erythrocytes of patients with chronic cholestasis and in healthy subjects. 2. The membranes from the patients contained more cholesterol and phospholipid and had a higher cholesterol/phospholipid molar ratio than the membranes from the healthy subjects. 3. The sodium efflux rate constant was reduced in the patients and this was entirely due to a reduction in the frusemide-sensitive efflux rate constant. There was no difference in either the ouabain-sensitive or the ouabain plus frusemide-resistant rate constants. 4. This reduction in the frusemide-sensitive rate constant was associated with a reduction in the erythrocyte sodium content. 5. When erythrocytes were loaded with cholesterol in vitro the frusemide-sensitive efflux rate constant was reduced by an amount similar to that observed in the patients. In addition, however, there was a reduction in the ouabain-sensitive efflux rate constant and an increase in the erythrocyte sodium content; neither of these changes was observed in the patients in vivo.

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