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.

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.

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 Acute and Chronic Salt Loading on Erythrocyte 22Na Efflux in Males with Essential Hypertension

1981 ◽  
Vol 61 (s7) ◽  
pp. 37s-39s ◽  
Author(s):  
J. B. Myers ◽  
W. R. Fitzgibbon ◽  
T. O. Morgan
Keyword(s):  
Essential Hypertension ◽  
Rate Constant ◽  
Sodium Transport ◽  
Sodium Intake ◽  
Efflux Rate ◽  
Natriuretic Hormone ◽  
Salt Loading ◽  
Sodium Efflux ◽  
Plasma Factor ◽  
Efflux Rate Constant

1. Present results confirm our previous work which showed that a sodium intake over 3 mmol day−1 kg−1 decreased the total erythrocyte efflux rate constant in untreated males with essential hypertension. 2. The infusion of saline (2.25 mmol of Na+/kg) over 30 min decreased the efflux rate constant. 3. The change after chronic sodium loading and the intravenous infusion of saline is in the ouabain-sensitive component (ouabain-sensitive Na+, K+ ATPase pump activity) of total efflux. 4. The reduction in efflux by an acute sodium load occurred only when chronic sodium intake was low. 5. Posture did not affect the efflux rate constant whether sodium intake was high or low. 6. The reduction in efflux after chronic ingestion and acute administration of sodium occurred only when erythrocytes were incubated in plasma. It did not occur in artificial medium, which suggested that a plasma factor mediated the effect of added sodium on cell sodium efflux. 7. The effect of sodium on cell sodium transport by a plasma factor with ouabain-like properties (which may be a natriuretic hormone) constitutes a regulatory system. This system, the sodium-ouabain-vsensitive cell sodium-transport pathway system, has important implications for the understanding of blood pressure control and sodium homeostasis.

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.

Effect of Zinc on Leucocyte Sodium Transport In Vitro

1978 ◽  
Vol 54 (5) ◽  
pp. 585-587 ◽  
Author(s):  
J. Patrick ◽  
J. Michael ◽  
M. N. Golden ◽  
B. E. Golden ◽  
P. J. Hilton
Keyword(s):  
Tissue Culture ◽  
Sodium Transport ◽  
Zinc Concentration ◽  
Culture Fluid ◽  
Sodium Content ◽  
Cell Water ◽  
Sodium Influx ◽  
Sodium Efflux

1. In a preparation of human leucocytes maintained in tissue culture fluid, increasing the extracellular zinc concentration leads to a significant increase in both ouabain-sensitive sodium efflux and in sodium influx. 2. Cell water and sodium content do not alter significantly with increasing extracellular zinc concentration. 3. A small increase in the ouabain-insensitive sodium efflux can be demonstrated when the external zinc concentration is raised from 0·75 μmol/l to 90 μmol/l.

Effects of Serum from Patients with Fulminant Hepatic Failure on Leucocyte Sodium Transport

1982 ◽  
Vol 63 (3) ◽  
pp. 237-242 ◽  
Author(s):  
R. B. Sewell ◽  
R. D. Hughes ◽  
Lucilla Poston ◽  
Roger Williams
Keyword(s):  
Fulminant Hepatic Failure ◽  
Sodium Transport ◽  
Hepatic Failure ◽  
Elution Profile ◽  
Sodium Efflux ◽  
Polyacrylonitrile Membrane ◽  
Normal Controls

1. Serum from patients with fulminant hepatic failure inhibits the ouabain-sensitive sodium efflux in leucocytes. A 1:100 dilution of the serum was necessary before the inhibition became undetectable. 2. Dialysates of the serum through cuprophane in vitro and polyacrylonitrile haemodialysis in vivo were inhibitory in small amounts. 3. Ultrafiltrates (<10 000 daltons) of serum were chromatographed on Sephadex G-25 and the elution profile obtained from patients with fulminant hepatic failure was both qualitatively and quantitatively different from that of normal controls. Material from peaks 3, 4, 5 and 7 in patients with fulminant hepatic failure inhibited leucocyte sodium transport. 4. The dialysate from haemodialysis with the polyacrylonitrile membrane contained most peaks, particularly peaks 4 and 5. Adsorption of serum with polymer coated charcoal in vitro largely removed peaks 5−8.

Abnormal Sodium Transport in Leucocytes from Patients with Essential Hypertension and the Effect of Treatment

1974 ◽  
Vol 48 (s2) ◽  
pp. 169s-170s ◽  
Author(s):  
R. D. Thomas ◽  
R. P. S. Edmondson ◽  
P. J. Hilton ◽  
N. F. Jones
Keyword(s):  
Essential Hypertension ◽  
Rate Constant ◽  
Sodium Transport ◽  
Sodium Efflux ◽  
Accelerated Hypertension ◽  
Effect Of Treatment ◽  
Sodium Metabolism ◽  
Water Contents

1. In seventeen patients with untreated essential hypertension the sodium and water contents of leucocytes were significantly increased, whereas the rate constant for ouabain-sensitive sodium efflux was significantly reduced. 2. These abnormalities were not found in fourteen other patients with well-controlled hypertension. 3. Preliminary observations in accelerated hypertension suggest a different pattern of abnormality in leucocyte sodium metabolism.

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.

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.

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