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

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.

1981 ◽  
Vol 61 (s7) ◽  
pp. 37s-39s ◽  
Author(s):  
J. B. Myers ◽  
W. R. Fitzgibbon ◽  
T. O. Morgan

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.


1975 ◽  
Vol 49 (3) ◽  
pp. 213-216 ◽  
Author(s):  
R. P. S. Edmondson ◽  
P. J. Hilton ◽  
N. F. Jones ◽  
J. Patrick ◽  
R. D. Thomas

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.


1988 ◽  
Vol 75 (6) ◽  
pp. 577-579 ◽  
Author(s):  
J. F. Morris ◽  
L. Poston ◽  
C. D. Wolfe ◽  
P. J. Hilton

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.


1984 ◽  
Vol 66 (3) ◽  
pp. 365-368
Author(s):  
Kevin Morgan ◽  
M. Afzal Mir

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.


1987 ◽  
Vol 73 (3) ◽  
pp. 291-297 ◽  
Author(s):  
J. F. Morris ◽  
M. D. McEachern ◽  
L. Poston ◽  
S. E. Smith ◽  
M. J. Mulvany ◽  
...  

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.


1985 ◽  
Vol 68 (2) ◽  
pp. 239-241 ◽  
Author(s):  
H. H. Gray ◽  
L. Poston ◽  
V. E. Johnson ◽  
P. J. Hilton

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.


1982 ◽  
Vol 63 (s8) ◽  
pp. 65s-67s ◽  
Author(s):  
R. B. Jones ◽  
J. Patrick ◽  
P. J. Hilton

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.


BMJ ◽  
1984 ◽  
Vol 288 (6418) ◽  
pp. 673-675 ◽  
Author(s):  
H H Gray ◽  
L Poston ◽  
P J Hilton ◽  
S J Smith ◽  
N D Markandu ◽  
...  

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