Cell Sodium, Potassium and Water in Uraemia and the Effects of Regular Dialysis as Studied in the Leucocyte

1974 ◽  
Vol 46 (5) ◽  
pp. 583-590 ◽  
Author(s):  
J. Patrick ◽  
N. F. Jones
Keyword(s):  
Renal Failure ◽  
Important Determinant ◽  
Potassium Concentration ◽  
Normal Subjects ◽  
Sodium Content ◽  
Intracellular Sodium ◽  
Potassium Content ◽  
Cell Water ◽  
Sodium Potassium ◽  
Water Contents

1. The leucocyte has been used as a model for the study of intracellular sodium, potassium and water in uraemia. The advantages of this cell are described. 2. In undialysed patients with advanced renal failure leucocyte sodium and water contents were significantly greater than normal. Leucocyte potassium content (mmol/kg of dry solids) and concentration (mmol/l of cell water) were reduced. 3. In patients receiving regular dialysis leucocyte water was significantly reduced. Leucocyte potassium content was also reduced in this group, but leucocyte potassium concentration in cell water had returned to normal. 4. In the normal subjects and also in the dialysed patients leucocyte water correlated better with potassium than with sodium content. In contrast, in the undialysed uraemic patients leucocyte water correlated better with sodium than with potassium content, indicating that the increased cell sodium was an important determinant of the increased cell water in this group.

WATER AND ELECTROLYTE CONTENT OF SKELETAL MUSCLE IN ACROMEGALY

1965 ◽  
Vol 48 (3) ◽  
pp. 469-472 ◽  
Author(s):  
Genaro Palmieri ◽  
Denis Ikkos
Keyword(s):  
Skeletal Muscle ◽  
Chloride Content ◽  
Sodium Content ◽  
Intracellular Sodium ◽  
Potassium Content ◽  
Sodium Potassium ◽  
Electrolyte Content

ABSTRACT Measurements of the fat, water, sodium, potassium and chloride content of muscle were performed in biopsies obtained from nine unselected acromegalic patients. The water, sodium and chloride contents were normal, while the potassium content was significantly increased (P < 0.01) by eight per cent. These results were interpreted as showing that the intracellular sodium content of the muscle is normal in acromegaly and that there is no extracellular oedema in this disease.

The Response of the Human Leucocyte to Alterations in Extracellular Osmolality

1973 ◽  
Vol 44 (5) ◽  
pp. 457-465 ◽  
Author(s):  
J. Patrick ◽  
P. J. Hilton
Keyword(s):  
Water Content ◽  
Sodium Content ◽  
Passive Movement ◽  
Human Erythrocytes ◽  
Intracellular Sodium ◽  
Potassium Content ◽  
Sodium Potassium ◽  
Permeable Membrane ◽  
Sodium And Potassium

1. The effect of variations in extracellular osmolality from 249 to 345 mosmol/kg upon the sodium, potassium and water content of human leucocytes has been studied. 2. Similar studies were performed using human erythrocytes. 3. Changes in the leucocyte water content were not explicable in terms of passive movement of water across an ‘ideal’ semi-permeable membrane. 4. Hypo-osmolal swelling was associated with a rise in intracellular sodium content and hyperosmolal shrinkage was associated with a fall in intracellular sodium content. 5. There were no significant changes in sodium and potassium content of the erythrocyte with altered external osmolality.

Aorta Electrolytes of Hypotensive Potassium-Deficient Rats

1958 ◽  
Vol 195 (2) ◽  
pp. 445-447 ◽  
Author(s):  
S. Charles Freed ◽  
Shirley St. George ◽  
Ray H. Rosenman
Keyword(s):  
Blood Pressure ◽  
Potassium Concentration ◽  
Pressure Rise ◽  
Sodium Concentration ◽  
Sodium Content ◽  
Potassium Deficiency ◽  
Sodium Potassium ◽  
High Sodium ◽  
Blood Pressure Rise ◽  
Arterial Tone

The hypotension of potassium-deficiency is associated with a decrease in aorta potassium concentration, the sodium content remaining unchanged, resulting in a high sodium/potassium ratio. Loss of arterial tone may result and thus contribute to the lowering of blood pressure. Cortisone administration to such rats does not alter the low aorta potassium content but appreciably reduces the sodium concentration. The return to a more normal sodium/potassium ratio in the aorta following cortisone may restore the arterial tone and thus explain the blood pressure rise to normal levels.

Distribution of Intracellular Sodium, Potassium and Chloride in Arenicola Marina Equilibrated to Diluted Sea Water

1985 ◽  
Vol 65 (2) ◽  
pp. 395-413 ◽  
Author(s):  
R. F. H. Freeman ◽  
T. J. Shuttleworth
Keyword(s):  
Cell Volume ◽  
Sea Water ◽  
Intracellular Sodium ◽  
Cell Water ◽  
Sodium Potassium ◽  
Arenicola Marina ◽  
Osmotic Equilibrium ◽  
Full Strength ◽  
Inorganic Solutes ◽  
Simultaneous Loss

In some earlier papers we have discussed the distribution of water and the total amounts of the major inorganic solutes in the cells of Arenicola marina (L.) equilibrated to full-strength and to diluted sea water (Freeman & Shuttleworth 1977b, c). We concluded that adaptation to dilute media by this osmoconforming worm was dependent entirely upon the regulation of cell volume. In dilute media substantial amounts of water do enter the cells but down to about 30% sea water this is only 55% of that which would have entered if the osmotic equilibrium was accomplished by entry of water alone. The influx of water is restrained by simultaneous loss of solute, an increasing amount of solute being lost or rendered osmotically inactive as the dilution increases. For lugworms in 35% sea water, for example, the volume of cell water has doubled compared with worms in 100% sea water, but the increase would have been far greater if the intracellular solutes had not declined by 30%.

Erythrocyte Sodium and Potassium in Patients with Hypokalaemia

1983 ◽  
Vol 64 (2) ◽  
pp. 167-176 ◽  
Author(s):  
M. Cumberbatch ◽  
D. B. Morgan
Keyword(s):  
Potassium Concentration ◽  
Sodium Content ◽  
Potassium Content ◽  
Extracellular Potassium ◽  
Moderate Degree ◽  
Sodium Efflux ◽  
Erythrocyte Sodium ◽  
Curvilinear Relation ◽  
Sodium And Potassium

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.

Observations on the Measurement and Regulation of the Sodium Content of Human Erythrocytes

1972 ◽  
Vol 42 (4) ◽  
pp. 447-453 ◽  
Author(s):  
E. K. M. Smith
Keyword(s):  
Linear Correlation ◽  
Sodium Pump ◽  
Potassium Concentration ◽  
Normal Subjects ◽  
Sodium Concentration ◽  
Sodium Content ◽  
Active Sodium ◽  
Sodium Efflux ◽  
Precise Control ◽  
A Cell

1. The sodium concentration within the erythrocytes of 159 subjects was found to be 7·35 ± 1·25 (SD) mmol/litre of cells. 2. In 157 normal subjects, the erythrocyte potassium concentration was 99·08 ± 5·3 (SD) mmol/litre of cells. 3. In the erythrocytes from twenty-seven normal subjects there was a striking linear correlation between the rate constant for active sodium efflux and resting sodium concentration. 4. It is concluded that these studies confirm the assumption that the resting concentration of sodium within a cell is determined by the activity of the sodium pump. What is not known is the mechanism by which this precise control is maintained.

ZUR WIRKUNG VON ALDOSTERON UND CORTICOSTERON AUF DEN ELEKTROLYT- UND WASSERGEHALT BINDEGEWEBIGER ORGANE DER RATTE

1964 ◽  
Vol 46 (1) ◽  
pp. 47-64 ◽  
Author(s):  
Walter Kriegel ◽  
Wilhelm Dirscherl
Keyword(s):  
Water Content ◽  
Interstitial Water ◽  
Sodium Content ◽  
Significant Loss ◽  
Interstitial Space ◽  
Interstitial Tissue ◽  
Connective Tissues ◽  
Sodium Potassium ◽  
Water Contents ◽  
And Cartilage

ABSTRACT An attempt was made to elucidate the distribution of electrolytes and water in connective tissues of the rat by estimating the sodium, potassium and water content in muscle, liver, skin, cartilage, aorta, tendon and serum. Animal groups treated in the following manner were compared: 1. replacement of drinking water by 0.9 % saline, 2. adrenalectomy, 3. adrenalectomy and saline, 4. adrenalectomy, saline and treatment with aldosterone (25 μg d-aldosterone-monoacetate per day), 5. adrenalectomy, saline and treatment with corticosterone (2—4 mg per day). In the tissues investigated the electrolyte and water contents varied independently and differently in some cases. Sodium content or sodium depots respectively of the tissues were influenced in a variable manner. After administration of saline there was even a significant loss of amounts of sodium in the tendon and aorta of normal animals. After adrenal-ectomy and the development of severe insufficiency, the sodium content apart from the interstitial space of cellular tissues, was lowered only in the aorta. Moreover, adrenal insufficiency, partly compensated by administration of saline, led to loss of sodium in skin and cartilage, the latter loosing the largest relative amount. Treatment of adrenalectomized animals with aldosterone normalized the sodium content in all the connective tissues and caused retention of sodium in the cellular tissues. Adrenalectomized animals showed an increased water content in the connective as well as in the cellular tissues. The interstitial water especially in cartilage did not appear to be bound very tightly. After treatment with aldosterone a retention of water (without simultaneous retention of sodium in the connective tissues) could be observed in all tissues, whereas corticosterone normalized the water content in the connective tissues. Potassium was found to be increased in all tissues of markedly deficient animals. In addition retention of K in the connective tissues (interstitial space) requires a simultaneous imbibition or loosening of the interstitial tissue.

Raised Intracellular Sodium Consequent to Sodium-Potassium-Dependent ATPase Inhibition Does Not Cause Myogenic Contractions of 150 μm Arteries from Rat and Guinea Pig

1982 ◽  
Vol 63 (s8) ◽  
pp. 45s-48s ◽  
Author(s):  
M. J. Mulvany ◽  
C. Aalkjær ◽  
H. Nilsson ◽  
N. Korsgaard ◽  
T. Petersen
Keyword(s):  
Guinea Pig ◽  
Rat Aorta ◽  
Sodium Content ◽  
Intracellular Sodium ◽  
Sodium Potassium ◽  
Small Vessels ◽  
Dependent Atpase ◽  
Resistance Vessels ◽  
Atpase Inhibition ◽  
Large Vessels

1. We have examined effects of inhibition of Na+,K+-dependent ATPase in large and small arterial ring preparations from rats and guinea pigs. 2. Ouabain (1 mmol/l) caused myogenic contraction of rat aorta and tail artery, but had no long-lasting effect on 150 μm mesenteric and 150 μm femoral resistance vessels over a 3 h period. Much lower concentrations of ouabain (1 μmol/l) caused contraction of guinea pig aorta, but had no effect on the mesenteric and femoral resistance vessels. 3. In the mesenteric resistance vessels, ouabain (1 mmol/l, rat vessels; 1 μmol/l, guinea pig vessels) caused the intracellular sodium content to rise over 2 h from approx. 13 mmol/l to approx. 60 mmol/l, and in the rat mesenteric resistance vessels this was associated with membrane depolarization from approx. −54 mV to approx. −30 mV after 3 h. 4. The results suggest that whereas Na+,K+-ATPase inhibition and consequent raised intracellular sodium may cause contraction of large vessels, this does not seem to be the case for small vessels. It therefore seems that further investigation is required before it is accepted that raised intracellular sodium is in itself a factor of importance in the etiology of hypertension.

Evidence for an Increased Generation of Prostacyclin in the Microvasculature and an Impairment of the Platelet α-Granule Release in Chronic Renal Failure

1988 ◽  
Vol 60 (02) ◽  
pp. 205-208 ◽  
Author(s):  
Paul A Kyrle ◽  
Felix Stockenhuber ◽  
Brigitte Brenner ◽  
Heinz Gössinger ◽  
Christian Korninger ◽  
...  
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Blood Clotting ◽  
Normal Subjects ◽  
Chronic Uraemia ◽  
Wall Interaction ◽  
End Stage ◽  
Granule Release

SummaryThe formation of prostacyclin (PGI2) and thromboxane A2 and the release of beta-thromboglobulin (beta-TG) at the site of platelet-vessel wall interaction, i.e. in blood emerging from a standardized injury of the micro vasculature made to determine bleeding time, was studied in patients with end-stage chronic renal failure undergoing regular haemodialysis and in normal subjects. In the uraemic patients, levels of 6-keto-prostaglandin F1α (6-keto-PGF1α) were 1.3-fold to 6.3-fold higher than the corresponding values in the control subjects indicating an increased PGI2 formation in chronic uraemia. Formation of thromboxane B2 (TxB2) at the site of plug formation in vivo and during whole blood clotting in vitro was similar in the uraemic subjects and in the normals excluding a major defect in platelet prostaglandin metabolism in chronic renal failure. Significantly smaller amounts of beta-TG were found in blood obtained from the site of vascular injury as well as after in vitro blood clotting in patients with chronic renal failure indicating an impairment of the a-granule release in chronic uraemia. We therefore conclude that the haemorrhagic diathesis commonly seen in patients with chronic renal failure is - at least partially - due to an acquired defect of the platelet a-granule release and an increased generation of PGI2 in the micro vasculature.

Endogenous digoxin-like immunoreactive factors: impact on digoxin measurements and potential physiological implications.

1985 ◽  
Vol 31 (9) ◽  
pp. 1525-1532 ◽  
Author(s):  
R Valdes
Keyword(s):  
Renal Failure ◽  
Liver Failure ◽  
Pregnant Women ◽  
Serum Proteins ◽  
Newborn Infants ◽  
Normal Subjects ◽  
Carrier Proteins ◽  
Third Trimester ◽  
Weakly Bound ◽  
Urine And Serum

Abstract Various laboratories have reported endogenous digoxin-like immunoreactive factor(s) (DLIF) in blood from patients in renal failure or liver failure, from newborn infants, and from third-trimester pregnant women. Similar immunoreactivity has been detected in amniotic fluid, in cord blood, and in urine and serum from normal subjects. The factor(s) giving rise to this immunoreactivity cross react with antibodies used in many currently available immunoassays for digoxin, sometimes causing apparent digoxin concentrations exceeding the therapeutic range obtained for exogenous digoxin, with consequent errors in measurement and in subsequent clinical interpretation of digoxin results. Here, I summarize findings in our laboratory and those of others. DLIF evidently exist in three states in serum: tightly protein-bound, weakly protein-bound, and unbound (free). In normal subjects, greater than 90% of the total DLIF in serum is tightly but reversibly bound to serum proteins and is not readily detectable by direct measurement of digoxin in serum with conventional immunoassays. However, there seems to be a redistribution of the more weakly bound and unbound components in patients with renal failure, pregnant women, and newborns. The increased values detected in these groups are ascribable to increased amounts of weakly bound and unbound DLIF rather than to increased total DLIF. Carrier proteins may play a prominent role in the transport of these factors in blood. I discuss the potential physiological and pharmacological implications of detecting endogenous immunoreactive factors that cross react with antibodies to drugs.

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