Evidence for an inhibitor of leucocyte sodium transport in the serum of neonates

1987 ◽  
Vol 73 (3) ◽  
pp. 291-297 ◽  
Author(s):  
J. F. Morris ◽  
M. D. McEachern ◽  
L. Poston ◽  
S. E. Smith ◽  
M. J. Mulvany ◽  
...  
Keyword(s):  
Rate Constant ◽  
Sodium Transport ◽  
Normal Subjects ◽  
High Concentration ◽  
Third Trimester ◽  
Sodium Efflux ◽  
Cord Serum ◽  
Resistance Vessels ◽  
Control Serum ◽  
Efflux Rate Constant

1. In confirmation of previous studies, serum obtained from cord blood demonstrated endogenous digoxin-like immunoreactivity (EDLI). Sera from pregnant women in the third trimester also demonstrated EDLI, which disappeared after delivery. 2. Cord serum inhibited the total sodium efflux rate constant of a mixed leucocyte preparation when compared with the effect of control serum. This inhibition resulted from a depression of the ouabain-sensitive (sodium pump) component of the rate constant. 3. An ultrafiltrate of the serum (mol. wt. < 30 000) also inhibited ouabain-sensitive leucocyte sodium transport when compared with filtrate obtained from control serum. 4. DHA-S Dehydroepiandrosterone sulphate (DHA-S) and cortisone, both present in high concentration in cord serum, demonstrated EDLI but did not affect leucocyte sodium transport in the cells of normal subjects. 5. DHA-S had no effect on sodium transport or vasoconstrictor activity in human omental resistance vessels. 6. It is concluded that EDLI of cord serum is associated with sodium transport inhibitory activity. This is unlikely to be attributable to DHA-S or cortisone.

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.

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.

Studies of Sodium Transport in Thymocytes of Rats with DOC/Salt Hypertension

1982 ◽  
Vol 63 (s8) ◽  
pp. 65s-67s ◽  
Author(s):  
R. B. Jones ◽  
J. Patrick ◽  
P. J. Hilton
Keyword(s):  
Rate Constant ◽  
Sodium Transport ◽  
Dry Weight ◽  
Sodium Content ◽  
Intracellular Sodium ◽  
Control Group ◽  
Efflux Rate ◽  
Sodium Influx ◽  
Sodium Efflux ◽  
Efflux Rate Constant

1. Sodium transport and intracellular sodium content were studied in thymocytes of rats made hypertensive by treatment for 4 or 8 weeks with deoxycorticosterone (DOC) and salt (DOC/salt). 2. The systolic blood pressure in the DOC/salt animals was 152 ± sem 3 and 189 ± 3 mmHg after 4 and 8 weeks' treatment respectively. This was significantly higher than pressures in their respective controls (124 ± 4 and 126 ± 5 mmHg), which had been given 1% sodium chloride solution (171 mmol/l) only. 3. The total sodium efflux rate constant in the DOC/salt rats was lower than that in the control group after 8 weeks of treatment (5.56 ± sem 0.21 vs 6.12 ± 0.11 h−1; P < 0.05) but not after 4 weeks of treatment (5.93 ± 0.13 vs 6.32 ± 0.13 h−1;0.1 > P > 0.05). 4. Intracellular sodium content in the DOC/salt rats was significantly higher than that of the control animals after 8 weeks' treatment (49.6 ± 2.5 vs 42.1 ± 1.0 mmol/kg dry weight; P < 0.05). 5. No significant changes were observed in intracellular potassium content, sodium influx or ouabain-insensitive sodium efflux rate constant.

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.

scholarly journals The effect of environmental temperature on prandial changes in leucocyte sodium transport in man

1989 ◽  
Vol 62 (3) ◽  
pp. 639-645 ◽  
Author(s):  
L. L. Ng ◽  
T. D. R. Hockaday
Keyword(s):  
Sodium Transport ◽  
Room Temperature ◽  
Environmental Temperature ◽  
Normal Subjects ◽  
Efflux Rate ◽  
Intracellular Electrolytes ◽  
Daily Energy ◽  
Na Efflux ◽  
Efflux Rate Constant ◽  
Environmental Temperatures

Cellular sodium transport via the Na+, K+-ATPase contributes significantly to daily energy expenditure. The effect of a meal on leucocyte Na+ transport and intracellular electrolytes was therefore investigated in lean normal subjects at room temperatures of 23° and 33°, to determine if the Na pump responds to the need for thermogenesis. In the fasting state, the ouabain-sensitive efflux rate which reflects active Na+ transport, and the intracellular electrolytes were similar. At 2 h after eating a 4·2 MJ (1000 kcal) meal, the ouabain-sensitive efflux rate constant rose when the room temperature was 23° but not at 33°. The ouabain-sensitive Na+ efflux rate, an index of active Na+ transport, 0rose post-prandially at 23° only. The post-prandial activation of leucocyte active Na efflux in normal subjects was blunted at higher environmental temperatures, when the need for thermogenesis was reduced.

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.

Leucocyte Sodium Transport in Uraemia

1975 ◽  
Vol 49 (3) ◽  
pp. 213-216 ◽  
Author(s):  
R. P. S. Edmondson ◽  
P. J. Hilton ◽  
N. F. Jones ◽  
J. Patrick ◽  
R. D. Thomas
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Rate Constant ◽  
Sodium Transport ◽  
Sodium Efflux ◽  
Control Subjects ◽  
Active Moiety ◽  
Total Sodium

1. In sixteen patients with severe chronic renal failure the rate constant for total sodium efflux from leucocytes was significantly reduced compared with that in thirty control subjects. This difference lay chiefly in the glycoside-sensitive (‘active’) moiety of sodium efflux. 2. In sixteen patients receiving regular haemodialysis, the rate constant for total sodium efflux from the leucocyte was significantly greater than in the undialysed uraemic patients though still subnormal. 3. In individual patients, an increase in sodium efflux could be detected as early as 1 week after regular haemodialysis was started. 4. These results are compatible with the existence of a dialysable molecule in uraemic plasma affecting leucocyte sodium transport.

Ouabain-Resistant, Frusemide-Sensitive Sodium Efflux in Human Lymphocytes: A Comparison of Normotensive and Hypertensive Subjects

1984 ◽  
Vol 67 (4) ◽  
pp. 407-411 ◽  
Author(s):  
A. Montanari ◽  
Isabella Simoni ◽  
E. Sani ◽  
P. Schianchi ◽  
A. Borghetti ◽  
...  
Keyword(s):  
Rate Constant ◽  
Human Lymphocytes ◽  
Sodium Content ◽  
Peripheral Blood Lymphocytes ◽  
Free Medium ◽  
Transport Pathway ◽  
Sodium Efflux ◽  
Low Sodium ◽  
Efflux Rate Constant ◽  
Cotransport System

1. Peripheral blood lymphocytes were isolated at room temperature in a low sodium medium in 17 normotensive control subjects (NC) and 13 patients with essential hypertension (EHP). 2. Lymphocyte sodium content was not significantly different between NC and EHP (3.1 ± 0.5, n = 11, and 3.6 ± 0.5, n = 10, respectively; means ± sem). 3. The effect of frusemide on the ouabain-resistant rate constant of sodium efflux (KNao) from these lymphocytes into a sodium-free medium was measured. 4. The frusemide-sensitive efflux rate constant was 75 ± 5 μs (n = 17) in controls and significantly lower in EHP (32 ± 7 μs, n = 13, P<0.001). 5. In human lymphocytes there is a ouabain-resistant, frusemide-sensitive fraction of sodium efflux into a sodium-free medium; this fraction may be reasonably attributed to a sodium-potassium cotransport system. This sodium transport pathway seems to be reduced in lymphocytes from EHP.

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