Erythrocyte Sodium and Potassium during the Development of Chronic Renal Failure in Rats

1985 ◽  
Vol 69 (s12) ◽  
pp. 13P-13P
Author(s):  
T.H. Thomas ◽  
C. Mason ◽  
K.M. Illingworth
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Erythrocyte Sodium ◽  
Sodium And Potassium

Erythrocyte Sodium during Erythropoiesis in Rats with Experimental Chronic Renal Failure

1983 ◽  
Vol 65 (3) ◽  
pp. 58P-58P
Author(s):  
C. Mason ◽  
K.M. Rowley ◽  
T.H. Thomas
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Erythrocyte Sodium

Erythrocyte Sodium and Hypertension in Chronic Renal Failure

1986 ◽  
Vol 4 (6) ◽  
pp. 798
Author(s):  
T H Thomas ◽  
H Mansy ◽  
R Wilkinson
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Erythrocyte Sodium

Erythrocyte Sodium Transport in Chronic Renal Failure

1982 ◽  
Vol 62 (5) ◽  
pp. 489-494 ◽  
Author(s):  
R. Swaminathan ◽  
G. Clegg ◽  
M. Cumberbatch ◽  
Z. Zareian ◽  
F. McKenna
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Atpase Activity ◽  
Healthy Subjects ◽  
Binding Capacity ◽  
Sodium Content ◽  
Ouabain Binding ◽  
Sodium Pumps ◽  
Group A ◽  
Erythrocyte Sodium

1. Erythrocyte sodium, sodium transport (ouabain-sensitive efflux rate of sodium, oMosNa, and ouabain-sensitive efflux rate constant of sodium, oMosNa), sodium-potassium activated ouabain-sensitive adenosine triphosphatase (Na+, K+-ATPase) activity and [3H]ouabain-binding capacity were measured in 15 patients with chronic renal failure and in 10 healthy subjects. 2. As a group, patients with chronic renal failure had a lower erythrocyte sodium and oMosNa compared with healthy subjects. 3. When patients were divided according to their erythrocyte sodium (greater or less than 4 mmol/kg of cells), in the group of patients whose erythrocyte sodium was less than 4 mmol/kg of cells (group A) the oMosNa was higher than that in healthy subjects and the oMosNa, Na+, K+-ATPase activity and [3H]ouabain-binding capacity were the same as those in healthy subjects. In the subgroup of patients with renal failure whose erythrocyte sodium content was greater than 4 mmol/kg of cells (group B) the oMosNa was less and plasma urea concentration higher than in group A and Na+, K+-ATPase activity, [3H]ouabain-binding capacity and oMosNa were lower than in healthy subjects. 4. These results suggest that in early chronic renal failure there is stimulation of ‘sodium pumps’ (without alteration in their number), which causes a lowering of erythrocyte sodium content, and that as the disease progresses there is inhibition of the ‘sodium pumps’ as well as a reduction in membrane permeability so that erythrocyte sodium is near normal.

Changing effects on erythrocyte sodium and potassium during the development of chronic renal failure with anaemia in rats

1986 ◽  
Vol 71 (6) ◽  
pp. 639-646 ◽  
Author(s):  
T. H. Thomas ◽  
C. Mason ◽  
K. M. Illingworth
Keyword(s):  
Renal Failure ◽  
Erythrocyte Membrane ◽  
Sodium Pump ◽  
Plasma Potassium ◽  
Plasma Urea ◽  
Sodium Flux ◽  
Erythrocyte Sodium ◽  
Erythrocyte Membrane Permeability ◽  
Sodium And Potassium ◽  
Erythrocyte Destruction

1. Rats were studied 7 days and 17 days after the onset of renal failure which was induced by a surgical technique. 2. Plasma urea, creatinine (PCr) and potassium had increased after 7 days; plasma potassium increased much more after 17 days but PCr was slightly lower. 3. Renal failure caused resetting of erythropoietic control to a lower level of packed cell volume (PCV). After 7 days renal failure some rats had a low PCV, whereas others still had a normal PCV apparently due to slower erythrocyte destruction of pre-renal failure cells. 4. After 7 days renal failure, rats with a normal PCV had an increased erythrocyte membrane leak to potassium that resulted in a low erythrocyte potassium [K+]RBC. This was accompanied by an increase in active sodium pump units [increased ouabain sensitive sodium flux (Fo) and its rate constant (ko)] that caused erythrocyte sodium ([Na+]RBC) to fall. The increased active pump units retarded the fall in [K+]RBC and may have extended the life of the normal erythrocytes in the renal failure environment. 5. The PCV was below normal in all rats after 17 days renal failure. [K+]RBC was increased and since ko was normal there appeared to be compensation to produce erythrocytes with reduced membrane leak to potassium with longer standing renal failure. 6. PCr was only related to PCV after 17 days renal failure and not in the earlier phase of erythrocyte destruction. The changes in erythrocyte membrane permeability were very significantly related to PCV after 17 days.

Relations between Sodium Transport and Sodium Concentration in Human Erythrocytes in Health and Disease

1981 ◽  
Vol 60 (5) ◽  
pp. 555-564 ◽  
Author(s):  
M. Cumberbatch ◽  
D. B. Morgan
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Membrane Permeability ◽  
Sodium Transport ◽  
Healthy Subjects ◽  
Total Activity ◽  
Sodium Content ◽  
Sodium Efflux ◽  
Sodium Pumps ◽  
Erythrocyte Sodium

1. We have examined the inter-relationships between erythrocyte sodium content and sodium transport in a group of healthy subjects and in groups of patients with disorders known to change the sodium content of erythrocytes. 2. In the healthy subjects the sodium content of erythrocytes was inversely related to both the permeability of the erythrocyte membrane to sodium (as measured by the unidirectional, ouabain-sensitive, sodium efflux) and the total activity of the sodium pumps (as measured by the rate constant of ouabain-sensitive sodium efflux). There was a correlation between the total activity of the sodium pumps and the membrane permeability to sodium. 3. Changes in the erythrocyte sodium content were due to a decrease in the activity of the sodium pumps (as in hypokalaemia and digoxin treatment), or a decrease in the permeability of the erythrocyte membrane to sodium (as in chronic renal failure) or a reduction of both the membrane permeability and the number of sodium pumps (as in hyperthyroidism or elderly patients). 4. One interpretation of the results in the healthy subjects is that there are two components of sodium influx; one associated with the sodium pumps in what we have called ‘membrane-units’ and the other determined by the ground permeability of the membrane. 5. On the basis of this model we suggest that in the geriatric and hyperthyroid patients there is a reduction in the number of ‘membrane-units’, that in hypokalaemia and during digoxin treatment there is inhibition of the sodium-pump component of the ‘membrane-units’ and that in chronic renal failure there is a decrease in the permeability of the membrane to sodium.

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