The Effects of Plasma from Normal Subjects Taking Low and High Salt Diets on the Erythrocyte Sodium Pump

1983 ◽  
Vol 65 (3) ◽  
pp. 66P-66P
Author(s):  
P.L. Weissberg ◽  
M.J. West ◽  
M.R. Wilkins
1990 ◽  
Vol 79 (6) ◽  
pp. 625-630 ◽  
Author(s):  
T. H. Thomas ◽  
S. MacPhail ◽  
V. Mott ◽  
R. Wilkinson

1. Young and mature erythrocytes from 15 normal subjects were used to compare the sodium pump rate constant measured in whole blood with the more definitive sodium affinity constant and maximum velocity of the sodium pump measured in artificial media using sodium-loaded cells. 2. Similar values were obtained from both erythrocyte fractions for the sodium affinity constant and maximum velocity and also by using two different plots. The median error in the estimate of individual sodium affinity constants and maximum velocities from regression analysis was about 20% and the precision was not improved by combining the data points for the two erythrocyte fractions. 3. The rate constant in whole blood was closely related to the sodium affinity constant and maximum velocity of the sodium pump (r = 0.75), suggesting that it was a reasonable overall assessment of available sodium pump activity. 4. Differences in the rate constant between subjects were due to differences in both the maximum velocity and sodium affinity constant of the sodium pump so that the rate constant could not be used as a guide to the underlying sodium pump physiology.


1984 ◽  
Vol 67 (2) ◽  
pp. 195-203 ◽  
Author(s):  
Christopher S. Wilcox ◽  
William E. Mitch ◽  
Ralph A. Kelly ◽  
Paul A. Friedman ◽  
Paul F. Souney ◽  
...  

1. We investigated the effects of Na+ intake, the renin-angiotensin-aldosterone system and antidiuretic hormone (ADH) on K+ balance during 3 days of frusemide administration to six normal subjects. Subjects received 40 mg of frusemide for 3 days during three different protocols: Na+ intake 270 mmol/day (high salt); Na+ intake 20 mmol/day to stimulate the renin-angiotensin-aldosterone system (low salt); Na+ intake 270 mmol/day plus captopril (25 mg/6 h) to prevent activation of the renin-angiotensin-aldosterone system. In a fourth protocol, a water load was given during high salt intake to prevent ADH release and then frusemide was given. 2. During high salt intake, frusemide increased K+ excretion (UKV) over 3 h, but the loss was counterbalanced by subsequent renal K+ retention so that daily K+ balance was neutral. 3. During low salt intake, the magnitude of the acute kaliuresis following the first dose of frusemide and the slope of the linear relationship between UKV and the log of frusemide excretion were increased compared with that found during the high salt intake. In addition, low salt intake abolished the compensatory renal retention of K+ after frusemide and cumulative K+ balance over 3 days of diuretic administration was uniformly negative (−86 ± 7 mmol/3 days; P < 0.001). 4. Captopril abolished the rise in plasma aldosterone concentration induced by frusemide. The acute kaliuresis after frusemide was unchanged compared with that observed during high salt intake. The compensatory reduction in UKV occurring after the diuretic was slightly potentiated. In fact, captopril given without the diuretic induced a small positive K+ balance. 5. When a water load was given concurrently with frusemide, the acute kaliuresis was >30% lower compared with that seen with frusemide alone, even though the natriuretic response was unchanged. 6. We conclude that: (a) K+ balance is maintained when frusemide is given during liberal Na+ intake because acute K+ losses are offset by subsequent renal K+ retention; (b) this compensatory K+ retention can be inhibited by aldosterone release which could account for the negative K+ balance seen during salt restriction; (c) the short-term kaliuretic response to frusemide is augmented by release of both ADH and aldosterone whereas changes in K+ balance over 3 days of frusemide are dependent on plasma aldosterone concentration.


1983 ◽  
Vol 56 (5) ◽  
pp. 925-929 ◽  
Author(s):  
Bruce M. Simat ◽  
Robert R. Mayrand ◽  
Arthur H. L. From ◽  
John E. Morley ◽  
Charles Billington ◽  
...  

1994 ◽  
Vol 170 (2) ◽  
pp. 693-698 ◽  
Author(s):  
Lesley M. Bolton ◽  
Trevor H. Thomas ◽  
Sheila Macphail ◽  
William Dunlop

1977 ◽  
Vol 7 (2) ◽  
pp. 229-233 ◽  
Author(s):  
G. J. Naylor ◽  
A. Smith ◽  
L. J. Boardman ◽  
D. A. T. Dick ◽  
E. G. Dick ◽  
...  

synopsisChanges in the erythrocyte membrane cation carrier following lithium ingestion in normal human subjects were studied; ouabain sensitive potassium influx fell significantly during the lithium treated phase. Lithium was fed to rats and no change in erythrocyte Na-K ATPase was shown. These findings contrast with studies of lithium in manic depressive psychosis. The fluctuations in the erythrocyte membrane cation carrier were studied in 5 normal subjects over 12 weeks and the correlations between the parameters calculated. The erythrocyte sodium concentration correlated positively with the ouabain sensitive potassium influx. This too contrasts with findings in manic depressive psychosis.


1985 ◽  
Vol 69 (s12) ◽  
pp. 44P-45P
Author(s):  
P.E. Jennings ◽  
M.R. Wilkins ◽  
M.J. West ◽  
M.J. Kendall ◽  
A.H. Barnett

1977 ◽  
Vol 76 (3) ◽  
pp. 399-401 ◽  
Author(s):  
Mabel Hokin-Neaverson ◽  
David A. Spiegel ◽  
William A. Burckhardt ◽  
James W. Jefferson

1989 ◽  
Vol 77 (s21) ◽  
pp. 29P-29P
Author(s):  
S MacPhail ◽  
T Thomas ◽  
R Wilkindson ◽  
JM Davison ◽  
W Dunlop

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