Erythrocyte Sodium and Potassium in Patients with Hypokalaemia

1983 ◽  
Vol 64 (2) ◽  
pp. 167-176 ◽  
Author(s):  
M. Cumberbatch ◽  
D. B. Morgan

1. The erythrocyte content of sodium and of potassium were measured in 231 unselected patients with hypokalaemia, and together with net ouabain-sensitive sodium efflux in patients with severe hypokalaemia, before (20 patients) and during potassium repletion (14 patients). 2. The erythrocytes of the patients with hypokalaemia compared with control subjects had on average an increase in sodium content, a decrease in potassium content and a reduction in the rate constant of ouabain-sensitive sodium efflux. All three changes had a similar curvilinear relation to the concentration of potassium in plasma with relatively little change in the measured variable unless the plasma potassium was very low. 3. There was a similar curvilinear relation between the final sodium and potassium content of normal erythrocytes and the potassium concentration of the medium in which they were incubated for 48 h in vitro. 4. These results suggest that the changes in the sodium and potassium content of erythrocytes in hypokalaemia are due to a direct inhibiting effect of the hypokalaemia on the activity of the sodium pump. 5. In many patients with hypokalaemia of moderate degree the increase in erythrocyte sodium content was less than expected from the effect in vitro of a low extracellular potassium concentration. This finding suggests that a compensatory change, presumably an increase in the number of sodium pumps, is a common event even in moderate hypokalaemia.

1981 ◽  
Vol 61 (3) ◽  
pp. 307-312 ◽  
Author(s):  
R. B. Jones ◽  
J. Patrick ◽  
P. J. Hilton

1. The effect of extracellular potassium on the transport of sodium and potassium in rat thymocytes has been studied in vitro. 2. A significant increase in the rate constant for total and ouabain-sensitive sodium efflux was demonstrated at an extracellular potassium concentration of 1 mmol/l as compared with that at either 0 or 2 mmol/l. 3. At potassium concentrations below 3 mmol/l ouabain-sensitive sodium influx was observed suggesting sodium-sodium exchange catalysed by the sodium pump. 4. Both total and ouabain-insensitive potassium efflux rose with external potassium. A small ouabain-sensitive potassium efflux was observed at all levels of external potassium studied. 5. Total and ouabain-insensitive potassium influx increased with external potassium, but did not appear to saturate. Ouabain-sensitive potassium influx reached a maximum at an external potassium concentration of 2 mmol/l then decreased with increasing external potassium.


1989 ◽  
Vol 76 (2) ◽  
pp. 199-203 ◽  
Author(s):  
R. Seon ◽  
T. Forrester

1. One hundred and five primigravidae were followed sequentially at 4-weekly intervals starting at gestational week 31. They were seen again at 6 weeks post partum. 2. At each visit measurements were made of blood pressure as well as of leucocyte and erythrocyte sodium and potassium content. 3. Eighty-five subjects completed the study. Seven developed pre-eclampsia. 4. In both controls and patients who developed preeclampsia, leucocyte and erythrocyte sodium content increased with gestational age and fell post partum. These changes were of greater magnitude in the patients with pre-eclampsia. Cell potassium fell in both groups, but to a greater extent in patients with pre-eclampsia. 5. These changes in cell sodium paralleled those in blood pressure in both groups. 6. These data suggest that the excessive blood pressure changes in pre-eclampsia might be related to similar changes in cell sodium content.


1975 ◽  
Vol 49 (5) ◽  
pp. 385-390
Author(s):  
P. J. Hilton ◽  
R. P. S. Edmondson ◽  
R. D. Thomas ◽  
J. Patrick

1. Sodium and potassium transport rates in human leucocytes were measured in vitro at different external potassium concentrations. 2. At nominally zero external potassium concentrations, the ouabain-sensitive sodium efflux was reduced to less than 20% of its maximum value. There was evidence that under these conditions a ouabain-sensitive sodium-sodium exchange occurs. 3. Both total and ouabain-insensitive potassium influx increased with increasing external potassium concentration. The ouabain-sensitive potassium influx showed saturation. 4. Ouabain-insensitive potassium efflux was also stimulated by increasing the external potassium concentration, suggesting significant potassium-potassium exchange at physiological external potassium concentrations.


1958 ◽  
Vol 36 (3) ◽  
pp. 333-338 ◽  
Author(s):  
F. A. Sréter ◽  
Sydney M. Friedman

After running a distance of 100 meters in 7 minutes, untrained rats showed a rise in plasma potassium and a fall in plasma sodium as measured in tail vein samples. These changes are in accord with in vitro observations of the effects of exercise on isolated muscle preparations and similarly are taken to indicate a gain of sodium and a loss of potassium by the exercised muscles in the whole animal. Within 10 minutes of completion of the exercise, plasma sodium concentration was restored to normal while potassium was restored within 20 minutes. Exercise was accompanied by a fall in haematocrit, which remained low for up to 40 minutes. A period of 2 months of preliminary training modified the response to exercise. In these trained animals, a fall in sodium concentration occurred as before but the rise in potassium concentration was less in degree and the haematocrit did not change. It is suggested that the rate of increase of plasma potassium is an index of muscle efficiency while the height of plasma potassium is correlated with the fatigue limit of exercise.


1957 ◽  
Vol 190 (1) ◽  
pp. 104-108 ◽  
Author(s):  
D. Laurence Wilson

Viable rabbit leucocytes have been obtained in quantities sufficient to permit direct chemical analyses of intracellular sodium and potassium concentrations. Treatment in vitro either with cortisone (10 or 20 mg/l.) or with desoxycorticosterone glycoside (10–80 mg/l.) led to a fall in intracellular potassium concentration and a reciprocal rise in intracellular sodium. There was an associated rise in intracellular water. After cortisone, the absolute change in sodium concentration slightly exceeded the reciprocal change in potassium; after desoxycorticosterone glycoside, the reverse was true.


1957 ◽  
Vol 189 (3) ◽  
pp. 451-454 ◽  
Author(s):  
Louis Tobian ◽  
Paul D. Redleaf

Administration of desoxycorticosterone and NaCl resulted in an increased sodium and potassium content of the aorta in rats becoming severely hypertensive. Equivocally hypertensive animals on this regimen showed smaller increases in sodium and a decrease in potassium. Sodium restriction prevented both hypertension and changes in arterial wall chemistry from occurring in rats receiving desoxycorticosterone. Hypertension per se may be fundamentally associated with an increased potassium and sodium content in artery, as experimental renal hypertension is characterized by a similar electrolyte alteration.


1975 ◽  
Vol 38 (1) ◽  
pp. 163-170 ◽  
Author(s):  
M. C. Moore Ede ◽  
M. F. Brennan ◽  
M. R. Ball

Circadian rhythms of plasma potassium concentration and urinary potassium excretion persisted in three normal volunteers when diurnal variations in activity, posture, and dietary intake were eliminated for 3–10 days. Measurements of the arteriovenous difference in plasma potassium concentration across the resting forearm and of erythrocyte potassium concentration suggested that there is a net flux of potassium from ICF to ECF in the early morning and a reverse net flux later in the day. The total net ICF-ECF fluxes were estimated from the diurnal variations in extracellular potassium content corrected for dietary intake and urinary potassium loss. The net fluxes between ICF and ECF were found to be counterbalanced by the circadian rhythm in urinary potassium excretion. Desynchronization of these rhythms would result in marked fluctuations in extracellular potassium content. These findings suggest that some revision is required of the concept of basal state in potassium homeostasis.


1984 ◽  
Vol 4 (4) ◽  
pp. 599-609 ◽  
Author(s):  
J. D. Pickard ◽  
S. Perry

The circular contractile responses to various stimuli have been measured in segments of cerebral arteries (both middle cerebral and basilar) taken from dogs either 3 or 7 days following the cisternal injection of autologous blood under anaesthesia. The maximum contractile response to 5-hydroxytryptamine was increased significantly 7 days following subarachnoid haemorrhage; the response to noradrenaline also increased but not significantly at 7 days. The contractile response to a raised extracellular potassium concentration (25 and 100 m M) was slightly depressed by 7 days, and the response to a fall in extracellular pH was depressed by 43% both 3 and 7 days following subarachnoid haemorrhage. The ability of these arteries to handle a sodium load was also assessed. The arteries were sodium loaded for various periods of time in mock cerebrospinal fluid with a zero potassium concentration. On transfer to 25 m M potassium solution, the duration but not the magnitude of the initial relaxation phase prior to a final contraction was greater with increasing time spent in the zero potassium solution. Both the magnitude and the duration of this relaxation phase, which reflect in part the ability of the vascular smooth muscle to extrude the sodium load, were increased in arteries following subarachnoid haemorrhage when compared with control arteries. These results demonstrate that the altered reactivity of cerebrovascular smooth muscle following subarachnoid haemorrhage persists in vitro and is more than simply an enhanced response to biogenic amines.


1978 ◽  
Vol 54 (5) ◽  
pp. 585-587 ◽  
Author(s):  
J. Patrick ◽  
J. Michael ◽  
M. N. Golden ◽  
B. E. Golden ◽  
P. J. Hilton

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.


1995 ◽  
Vol 74 (2) ◽  
pp. 565-573 ◽  
Author(s):  
M. A. Perez-Pinzon ◽  
L. Tao ◽  
C. Nicholson

1. An in vitro slice model of ischemia was used to study changes in extracellular potassium concentration and diffusion properties in the stratum pyramidale of CA1 and CA3 regions of the hippocampus and in the cortex of the rat. Slices were submerged in artificial cerebrospinal fluid, and ischemia was induced by removing oxygen and glucose until anoxic depolarization occurred. 2. Extracellular potassium concentration was measured with a valinomycin-based ion-selective microelectrode. The bathing medium contained 5 mM potassium, and in vitro ischemia caused the potassium concentration to rise to 45 mM in CA1, 12 mM in CA3, and 32 mM in cortex. 3. Extracellular volume fraction and tortuosity were determined during normoxic conditions and in vitro ischemia by measuring the diffusion of tetramethylammonium. This cation was iontophoretically released into the extracellular space and its concentration as a function of time determined with an ion-selective microelectrode approximately 100 microns away from the source. 4. During normoxia the volume fraction was 0.14, 0.20, and 0.18, and tortuosity was 1.50, 1.57, and 1.62 in CA1, CA3, and cortex, respectively. These data confirm that the volume fraction of CA1 is smaller than in the two other regions. 5. During ischemia the volume fraction decreased to 0.05, 0.17, and 0.09 in CA1, CA3, and cortex, respectively. Only in CA3 did the tortuosity change significantly by increasing to 1.75. Because of limitations in the time resolution of the diffusion method, the changes in volume fraction and tortuosity during the anoxic depolarization phase of ischemia may have been underestimated.(ABSTRACT TRUNCATED AT 250 WORDS)


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