Cellular Potassium Content Research Articles

Hypoosmotic volume regulation of astrocytes in elevated extracellular potassium

Cellular volume and potassium contents were determined in rat astrocytes from primary culture following suspension in isoosmotic (269 mOsm) and hypoosmotic (136 mOsm) phosphate-buffered saline (PBS) containing various potassium concentrations. Within 1 min of suspension in hypoosmotic PBS, cells swelled to 135% of their volume in isoosmotic PBS. This initial swelling was not altered by varying the potassium concentration of the hypoosmotic PBS. After suspension in hypoosmotic PBS containing 3.2 mM potassium, a regulatory volume decrease (RVD) was observed. Higher concentrations of potassium in hypoosmotic PBS inhibited RVD following osmotic swelling. Cells swollen in hypoosmotic PBS containing 50 mM potassium continued to swell for 7 min, reaching a volume of 141% of their initial isoosmotic volume. After 7 min, these cells demonstrated a subsequent decrease in volume. The swelling observed between 1-7 min after suspension in hypoosmotic PBS containing 50 mM potassium was not affected by 10 microM gadolinium, 1 mM quinine, 1 mM DIDS (4,4'-diisothiocyanato-2,2'-stilbenedisulfonic acid), 1 mM SITS (4-acetamido-4'-isothiocyanato-2,2'-stilbenedisulfonic acid), 1 mM furosemide, or 100 microM bumetanide. Normal RVD was obtained in hypoosmotic PBS containing 50 mM potassium, if chloride was replaced with gluconate (but not nitrate) to reduce the extracellular K.Cl product to that of hypoosmotic PBS containing 3.2 mM potassium. The volume decrease seen between 7-30 min after exposure to hypoosmotic PBS containing 50 mM potassium was blocked by 1 mM DIDS, 1 mM SITS, or 1 mM furosemide. Cellular potassium content was elevated by approximately 60% after 7 min exposure to isoosmotic or hypoosmotic PBS containing 50 mM potassium. In hypoosmotic PBS, this increase in cellular potassium was reduced with replacement of chloride by gluconate, but not by nitrate. The results indicate that astrocytes swollen in PBS containing elevated potassium concentrations continue to swell, in part, by accumulation of potassium plus chloride mediated by an approach to Donnan equilibrium. Cotransport carriers or stretch-activated channels do not play a role in the enhanced swelling observed in hypoosmotic PBS containing 50 mM potassium. We suggest that a voltage-sensitive chloride channel mediates this continuation of cell swelling. This mechanism may be important in the persistent swelling of astrocytes observed in pathologic conditions such as trauma and seizures where extracellular potassium is elevated, or when other factors are present which may cause astroglial depolarization.

Assessment of cell-specific cytotoxic responses of the kidney to selected aromatic hydrocarbons

The present studies were conducted to assess cell-specific cytotoxic responses of the kidney to selected aromatic hydrocarbons (AHs) using in vitro culture systems of glomerular mesangial cells and cortical tubular epithelial cells. Primary cultures of glomerular mesangial cells or cortical tubular epithelial cells were treated for 24 hr with naphthalene (NAPH, 0.1–1000 μ m), 2-methylnaphthalene (2-MNAPH, 0.1–1000 μ m), benzo[ a]pyrene (B[ a]P, 0.3–300 μ m), pentachlorophenol (PCP, 0.1–1000 μ m), 2,3,7,8-tetrachlorodibenzo- p-dioxin (TCDD, 0.001–1 n m) or 2,3,7,8-tetrachlorodibenzofuran (TCDF, 0.005–5 n m). [ 3H]Thymidine incorporation into DNA, cellular potassium content, and lactate dehydrogenase (LDH) leakage were used as indices of cytotoxicity. Glomerular mesangial cells exposed to NAPH or 2-MNAPH (0.1–1000 μ m) exhibited [ 3H]thymidine incorporation profiles similar to those of the vehicle controls, whereas B[ a]P at all concentrations and PCP at 1000 μ m decreased [ 3H]thymidine incorporation in comparison with the controls. TCDD and TCDF increased [ 3H]thymidine incorporation relative to controls at 0.1 n m and 0.5 n m, respectively. Glomerular mesangial cells treated with NAPH or PCP exhibited decreased cellular potassium content and increased LDH leakage only at the 1000 μ m concentration. In tubular epithelial cells, treatment with NAPH (10 or 1000 μ m), 2-MNAPH (10 or 1000 μ m), B[ a]P (300 μ m), and PCP (10 or 1000 μ m) induced concentration-dependent decreases in [ 3H]thymidine incorporation relative to controls. In contrast, exposure of tubular epithelial cells to TCDD or TCDF did not modulate [ 3H]thymidine incorporation at any of the concentrations tested. A modest decrease in cellular potassium content and an increase in LDH leakage was observed at the 1000 μ m concentration of PCP in tubular epithelial cells. On the basis of these data, we conclude that renal glomerular mesangial cells and tubular epithelial cells exhibit differential cytotoxic response profiles to AHs.

Cardiac cell toxicity induced by 4-hydroperoxycyclophosphamide is modulated by glutathione.

Cardiac myocytes were exposed to 4-hydroperoxycyclophosphamide (4-HC, an activated derivative of cyclophosphamide) to assess whether early ionic events are associated with the dose limiting toxicity of this chemotherapeutic agent. Primary cultures of embryonic chick cardiac myocytes were grown to confluency and then exposed to a medium containing 4-HC. Cellular sodium, potassium, and calcium contents were measured by atomic absorption spectrophotometry and related to protein and ATP content. Pretreatment of the cultured heart cells with glutathione depleting or enhancing agents provided the basis for evaluating the involvement of glutathione in the 4-HC-induced cytotoxicity. Administration of 150 microM 4-HC to cardiac myocytes resulted in increases in cellular sodium and calcium contents and decreases in potassium, ATP, and protein contents. Pretreatment of cardiac myocytes with L-buthionine-SR-sulphoximine, a specific inhibitor of gamma-glutamylcysteine synthetase, depleted cellular glutathione to 12% of control and significantly reduced the minimum concentration of 4-HC causing cytotoxic changes. Conversely, elevation of cellular thiol content by the pretreatment of cardiac myocytes with glutathione monoethyl ester (but not glutathione) provided protection against 4-HC induced cytotoxicity. Cellular glutahione concentration can markedly influence the 4-HC induced changes in cellular ion content and ATP, which are early indicators of 4-HC induced cytotoxicity.

Photodynamic treatment of yeast cells with the dye Toluidine blue: all-or-none loss of plasma membrane barrier properties

Photodynamic treatment of Kluyveromyces marxianus with the sensitizer Toluidine blue leads to the loss of colony forming capacity. In this paper, the influence of this treatment on the barrier properties of the plasma membrane has been studied. Photodynamic treatment with the dye Toluidine blue resulted in efflux of potassium ions and E 260-absorbing material. Moreover, cells became stainable with erythrosine. It is concluded that the permeability change induced by photodynamic treatment proceeds in an all-or-none fashion. Treatment of this yeast strain, with the dye and light, also induced a diminution of the cell volume. This process is most likely not coupled to the cellular potassium content, but rather to the integrity of the vacuole. These data suggest that the vacuole has an important function in the maintenance of cell volume. Finally, it was observed that the loss of cell viability was not induced by the all-or-none loss of barrier properties.

Effects of peroral magnesium on plasma and skeletal muscle electrolytes in patients on long-term diuretic therapy

Twenty patients on long-term diuretic therapy for arterial hypertension and/or congestive heart failure were given a supplementary dose of 15 mmol magnesium aspartate hydrochloride per day for 6 months. Nineteen patients, fulfilling the same admission criteria as the treatment group, served as controls. The addition of magnesium aspartate hydrochloride resulted in a significant rise of the cellular potassium and magnesium content and in a significant decrease of both systolic and diastolic blood pressure. It is concluded that supplementation with magnesium aspartate hydrochloride may effectively prevent the diuretic induced disturbances of electrolyte balance.

Hyperkalemia: Disorders of Internal and External Potassium Balance

The serum potassium level is normally preserved de spite changes in potassium intake and output (the exter nal potassium balance) and changes in its distribution in the body (the internal potassium balance). External potassium homeostasis depends primarily on renal ex cretion of the daily exogenous potassium burden. Inter nal homeostasis depends on the extrarenal regulation of potassium. Skeletal muscle and liver are the dominant sites of that regulation. The two chief regulators of inter nal balance are insulin and catecholamines, the latter acting through β-adrenergic receptors. Acid-base bal ance and the cellular potassium content are other important regulators of internal balance. The major disorders of external balance are renal failure, hypo reninemic hypoaldosteronism, interstitial nephritis, and a variety of drugs that impair renal potassium excretion. The major disorders of internal balance are diabetes mellitus, acidosis, medications, and release of endoge nous potassium during vigorous exercise, traumatic muscle injury, or tumor lysis chemotherapy. These dis orders frequently result in troublesome elevations of serum potassium in the intensive care setting. Their re view in this article includes a thorough discussion of the evaluation and proper management of the hyperkalemic patient.

Decreased NA+, K+-ATPase Activity in Erythrocyte Membrane from Rheumatoid Arthritis Patients

The activity of the plasma membrane Na+/K+-ATPase and cellular sodium (Nai) and potassium (Ki) content were analysed in RBCs from 15 rheumatoid arthritis (RA) and 30 reference subjects (11 healthy controls, 12 osteoarthritis and 7 gouty patients). Na+/K+-ATPase activity was determined by measuring the inorganic phosphate (Pi) released by incubation in a reaction medium in the presence and absence of K ions or ouabain. Nai and Ki were measured with an ion-selective electrode analyser on the hemolysates, after washing the RBCs in 110 mM MgCl2. The Na/K-ATPase activity was significantly lower in RA patients than in both healthy controls and patients with osteoarthritis or gout. A slight but significant increase in Nai was observed in rheumatoid subjects. It is hypothesized that the decrease in the Na+/K+-ATPase activity in RA may be the result of a defective expression of membrane proteins, which is probably related to the altered cell sensitivity observed.

Cyclosporine augments receptor-mediated cellular Ca2+ fluxes in isolated hepatocytes.

The immunosuppressive agent, cyclosporine, has been found to augment receptor-stimulated calcium fluxes in isolated hepatocytes. After treatment of Quin 2-loaded hepatocytes with cyclosporine, both the amplitude and duration of the vasopressin-induced rise in the cytosolic free Ca2+ are increased. These effects are dependent upon the concentration and time of exposure of the cells to cyclosporine. Cyclosporine increases both 45Ca2+ influx across the plasma membrane and the cellular calcium content. The total cellular magnesium, sodium, and potassium contents are not affected by cyclosporine. However, cyclosporine treatment, per se, has no apparent effect on the cytosolic free Ca2+ concentration as assayed by Quin 2 fluorescence. The increase in total cell calcium is associated with progressive increases in the calcium content of the endoplasmic reticular and mitochondrial calcium pools. The vasopressin-induced net efflux of Ca2+ from hepatocytes was 2-fold greater after treatment with 10 micrograms/ml cyclosporine for 10 min, but the lag time prior to the onset of Ca2+ efflux was not affected. These results are interpreted on the basis of cyclosporine having a primary effect on increasing the permeability of the plasma membrane to Ca2+, thereby leading to an increase of the calcium content of the hormone-sensitive intracellular calcium pool.

The relationship between valinomycin-induced alterations in membrane phospholipid fatty acid turnover, membrane potential, and cell volume in the human erythrocyte.

The relationship between alterations in transmembrane potential, cell volume, and phospholipid fatty acid turnover has been examined in human erythrocytes by treating the cells with the monovalent cation ionophore valinomycin. Valinomycin increases the cellular uptake of tetra[3H]phenylphosphonium ion by erythrocytes, indicating membrane hyperpolarization, and causes net loss of potassium chloride and water from the cells leading to a decrease in cell volume. Treatment of erythrocytes with valinomycin also enhances incorporation of [9, 10-(3)H]oleic acid into phospholipids, primarily diacylphosphatidylethanolamine. After replacing intracellular chloride with sulfate and treating cells with the anion transport inhibitor 4,4'-diisothiocyanostilbene-2,2'-disulfonate, exposure to valinomycin results in uptake of tetra[3H]phenylphosphonium ion and stimulation of [9, 10-(3)H]oleic acid incorporation, but, because anion efflux is prevented, no decrease in cell volume occurs. When tetra[3H]phenylphosphonium ion uptake is also prevented by suspending these cells in 125 mM KCl to dissipate the transmembrane potassium gradient, valinomycin still enhances [9, 10-(3)H] oleic acid incorporation into phospholipid. These results suggest that the presence of valinomycin in the membrane directly alters phospholipid fatty acid turnover and that some of the effects of this ionophore on cellular function previously attributed to alterations in transmembrane potential or cellular potassium content may instead be due to altered phospholipid turnover. Since it is possible that valinomycin may directly perturb phospholipid fatty acid turnover in other cells, the possibility that valinomycin-induced alterations in cellular function are due to altered phospholipid turnover rather than membrane hyperpolarization or altered potassium content should be considered in the interpretation of studies employing this ionophore.

Effects of medium acetate on cellular volume in rabbit renal cortical slices.

Slices of rabbit renal cortex were incubated at 25 degrees C in media in which acetate replaced chloride. There was gross cellular swelling in isosmotic 132 mM-acetate medium, and this swelling was unique in that, with a normal medium potassium concentration, it was accompanied by a substantial increase in cellular potassium content. This accumulation of potassium, but not the cellular swelling, was dependent upon metabolism and inhibited by ouabain. This accumulation of potassium was not dependent upon the cellular swelling. It also occurred in a hyperosmotic acetate medium in which swelling was minimized. In isosmotic media, the cellular swelling was proportional to medium acetate concentration and was also affected markedly by medium pH, being greatest at an initial medium pH of 7.1 and least at pH 7.7. The swelling was reversed and cellular composition restored when tissue was re-incubated in NaCl medium. Ouabain (10(-3)M) largely prevented this recovery in volume. The results are consistent with plasma-membrane-based theories, on the assumption that membranes are much more permeable to undissociated acetic acid than they are to the acetate ion. They are inconsistent with the expectations of an alternative hypothesis (the association--induction hypothesis) which ascribes the maintenance of cellular composition to properties of cellular proteins and cellular water rather than to those of the plasma membrane. The results do not favour the suggestion that cellular swelling itself results in irreversible cellular damage. The results are consistent with the hypothesis that the ouabain-inhibitable Na-K-ATPase plays a major role in the regulation of cellular volume. No alternative metabolically dependent volume regulating mechanism need be postulated to explain them.

Cytotoxicity of isoproterenol to cultured heart cells: Effects of antioxidants on modifying membrane damage

Primary cultures of rat myocytes were used to study the cardiac damage induced by toxic doses of l-isoproterenol (ISO). Cultures were exposed to varying concentrations of ISO (2.4 × 10 −5, 1 × 10 −4, and 5 × 10 −4 m) for 0.5, 1.5, 4, and 12 hr. Mitochondrial membrane fragility, myocyte potassium content (as an index of sarcolemmal damage), and cellular glutathione content were used to evaluate cellular injury. A significant increase in mitochondrial fragility was observed 0.5 hr after treatment with 5 × 10 −4 M ISO. Lower doses caused an increase in mitochondrial fragility 1.5 hr after exposure. Longer durations of ISO exposure (4 and 12 hr) were necessary to decrease cellular potassium content. Glutathione levels were minimally affected by ISO. l-Ascorbic acid (5 × 10 −3 m) or sodium bisulfite (9.6 × 10 −4 m) were added to the cultures to determine if antioxidants prevent the toxicity caused by ISO. The presence of l-ascorbic acid or sodium bisulfite in ISO-treated myocyte cultures prevented the toxic changes in mitochondrial fragility and myocyte potassium content. The data indicate that antioxidants may be useful in reducing injury induced by toxic doses of ISO. Furthermore, mitochondrial injury may be involved significantly with the development of ISO-induced cardiotoxicity.

Skeletal muscle injury after magnesium depletion in the dog.

Magnesium deficiency was induced in a setting of an otherwise adequate diet in adult beagle dogs. Despite the development of severe hypomagnesemia (from 1.5 +/- 0.2 to 0.5 +/- 0.2 meq/liter) during the 10-wk study, Mg content of skeletal muscle fell only modestly (from 3.8 +/- 0.2 to 3.1 +/- 0.4, P less than 0.005, at 7 wk and 3.5 +/- 0.4 mM/100 g FFDS, NS, at 10 wk). The most pronounced muscle compositional changes were a loss of phosphorus (from 29.5 +/- 1.8 to 22.0 +/- 1.6, P less than 0.001, at 7 wk and 24.8 +/- 2.8 mM/100 G FFDS, P less than 0.001, at 10 wk) and gains of calcium (from 0.64 +/- 0.11 to 0.93 +/- 0.17, P less than 0.05, at 7 wk, and 0.85 +/- 0.26 mM/100 g FFDS, P less than 0.05, at 10 wk), sodium (from 13.2 +/- 2.6 to 22.9 +/- 4.7, P less than 0.001 at 7 wk and 17.8 +/- 2.0 meq/100 g FFDS, P less than 0.005, at 10 wk), and chloride (from 5.8 +/- 0.8 to 8.2 +/- 1.6, P less than 0.001, at 7 wk and 6.8 +/- 0.6 meq/100 g FFDS, P less than 0.05, at 10 wk). Cellular potassium content did not change (from 35.9 +/- 1.9 to 33.0 +/- 4.1, NS, at 7 wk and 36.3 +/- 2.0 meq/100 g FFDS, NS, at 10 wk). Muscle cell electrical hyperpolarization developed after 10 wk of Mg depletion. Convulsive seizures developed in three animals. Frank rhabdomyolysis in three animals and focal necrosis in four animals were present on terminal biopsy, with only four animals having completely normal histology.

Na+ transport properties of the peritubular membrane of cortical collecting tubule.

The effects of varying endogenous aldosterone levels on the passive and active properties of the peritubular membrane were studied. Rabbits that were fed either a low Na+ (normal K+) diet or a high Na+, low K+ diet increased or decreased plasma aldosterone, respectively. Tubules were dissected, filled with oil, and incubated in 0 K+ medium to increase intracellular sodium. Cellular sodium and potassium content was measured by helium-glow photometry. The degree to which cells accumulate sodium and lose potassium is a function not only of time of exposure but also of diet. Tubules from animals on a low Na+ diet are about 6 times more permeable to sodium than those from animals fed a high Na+ diet. When tubules were loaded with sodium and returned to a normal (5 mM K+) bathing medium, net sodium efflux and potassium influx occurred. The rate of sodium efflux by cortical collecting tubules dissected from animals on the low Na+ diet was 2.3 times greater than the efflux rate of tubules from animals on the high Na+ diet. These data suggest that high levels of endogenous aldosterone enhance sodium transport measured in vitro across the peritubular membrane of cortical collecting tubule.

Evidence for chloride dependent potassium and water transport induced by hyposmotic stress in erythrocytes of the marine teleost,Opsanus tau

Red blood cells of the marine teleost,Opsanus tau (oyster toadfish), were characterized as to their normal hemoglobin, ion and water contents. Cells were exposed to ouabain containing, hyposmotic salt solutions (osmolarity reduced to 2/3 of normal) in which the cation or anion composition was varied. It was found that the initial cell volume expansion due to water influx was independent of the anion present. However, a secondary volume reduction was dependent on the presence of chloride or bromide anions. During volume reduction, cellular potassium and chloride ion contents fell by about equal amounts. Potassium loss was commensurate to the total amount of potassium ions detected extracellularly about 1.5h after the initial osmotic shock. No major changes were seen in the cellular sodium ion contents. When chloride ions within the cells and in the suspending medium were replaced by nitrate, iodide or thiocyanate, the cells failed to return to volumes close to those of isosmotically suspended controls, and the cellular potassium content also remained constant. In hypotonic potassium chloride the cells failed to extrude potassium chloride and water, and hence retained their expanded volume. Neither potassium loss nor volume decrease occurred in cells swollen in hypotonic sodium chloride media containing furosemide or 4,4′ diisothiocyano-2,2′-stilbene-disulfonic acid (DIDS). These two compounds are known inhibitors of monovalent cation cotransport and anion self exchange, respectively, in mammalian red cells. Hence toadfish red cells respond to osmotic swelling primarily by activation of an ouabain-insensitive, chloride dependent potassium transport system which is sensitive to inhibition by furosemide and DIDS.

Relationship between plasma and cellular potassium content during potassium repletion.

The simultaneous effect of two weeks of potassium repletion therapy on the plasma concentration and total body content of potassium was assessed in seven patients with hypokalaemia. Glomerular filtration rate, renal plasma flow, and maximal urinary concentration were also measured both before and after therapy with potassium chloride. While the plasma potassium concentration quickly returned to normal, total body content of potassium remained depressed, emphasizing the unreliability of the plasma potassium concentration as an indicator of total body potassium status. Parameters of renal function measured in this study, which were depressed by potassium depletion, also did not alter with correction of the plasma potassium level. This suggests that these functions are primarily affected by cellular potassium content.

Effect of intracellular sodium on calcium uptake in isolated guinea-pig diaphragm and atria

(1) Effects of cellular sodium on the 45Ca uptake of isolated guinea-pig diaphragm and atria were studied. (2) Cellular sodium and calcium contents were higher in diaphragm compared to atria after incubating the tissues in normal Krebs-Henseleit solution. (3) Cellular sodium content in atria and diaphragm were reduced signficantly by incubating the tissues in high potassium Krebs-Henseleit solution ( K + = 34.7 mM ), while it was increased by incubating the tissues in the ice-cold low potassium and low calcium Krebs-Henseleit solution ( K + = 0.65 mM , Ca 2+ = 0.2 mM ). Cellular potassium content was changed inversely to the sodium content. (4) In atria, cellular content of calcium was not altered significantly by the above conditions. But in diaphragm, the cellular content of calcium was decreased slightly but significantly after incubation in the ice-cold low potassium and low calcium Krebs-Henseleit solution. (5) At normal cellular sodium levels, the 45Ca uptake of both tissues was similar. (6) The reduction of the cellular sodium content caused a significant decrease in the 45Ca uptake into both tissues. (7) When the cellular sodium content was increased in atrial preparations, a marked increase in the 45Ca uptake was observed. On the other hand, in diaphragm preparations, only a slight increase was observed, even when cellular sodium content was much higher than the normal level. (8) These results indicate that even when the intracellular sodium is increased by some physiological of pharmacological events, calcium influx through Na +/Ca 2+ exchange mechanism is very slight and slow in diaphragm.

Effect of magnesium deficiency and excess on renal tubular potassium transport in the rat.

1. Dietary magnesium deficiency is commonly associated with significant potassium depletion although the mechanisms responsible are unknown. Because the kidney has an important role in both magnesium and potassium homeostasis, clearance and micropuncture experiments were performed on thyroparathyroidectomized magnesium-deficient, normal and hypermagnesaemic rats to study the effect of body magnesium status on renal potassium handling. 2. Dietary magnesium restriction that reduced total-body magnesium by 30% did not alter renal potassium excretion despite a 10% reduction in total-body potassium. Graded magnesium infusions increased the fractional excretion of potassium in both magnesium-depleted and normal rats. However, the increase in the dietary depleted group was significantly less than in the control group (5-10 and then 13% compared with 7-19 and then 28% respectively). These changes in urine potassium excretion followed alterations in distal-tubule function. Parathyroid hormone did not alter potassium excretion in any of the experimental groups in contrast with its effect on magnesium excretion. 3. These data support the concept of distal tubular control of renal potassium homeostasis. The body magnesium status appears to exert some control over cellular potassium content and to alter indirectly distal-tubule potassium excretion.

Selective stimulation of erythrocyte membrane phospholipid fatty acid turnover associated with decreased cell volume.

Treatment of erythrocytes with the divalent cation ionophore A23187 results in net uptake of calcium and a calcium-dependent decrease in cellular potassium content and cell volume. These changes in membrane properties are associated with a selective stimulation of fatty acid incorporation into membrane phosphatidylethanolamine (PE). In this study the relationship between this selective stimulation of phospholipid fatty acid turnover and changes in calcium uptake, cellular potassium content, and cell volume has been examined by 1) preventing the calcium-dependent loss of potassium without abolishing calcium uptake and 2) altering cellular potassium content and cell volume without increasing net uptake of calcium by utilizing the monovalent cation inonophore nigericin or increasing the osmolarity of the buffer. It has been shown that treatment of erythrocytes with A23187, nigericin, or hypertonic buffer results in a selective stimulation of fatty acid incorporation into PE. These results suggest that a mechanical or conformational change in the membrane is associated with a selective stimulation of fatty acid turnover in phosphatidylethanolamine.

Ventricular extrasystoles and intracellular electrolytes before and after potassium and magnesium infusions in patients on diuretic treatment

Thirty-four patients suspected of being magnesium deficient were given intravenous infusions of potassium and magnesium. The muscle contents of sodium, potassium, magnesium, and chloride were determined by atomic absorption spectrophotometry on skeletal muscle samples obtained by percutaneous biopsies. The frequency of ventricular etopic beats (VEBs) was assessed from a 3-hour ECG tape recording before the infusions and after the completion of each infusion. The potassium infusions did not result in any changes in the cellular potassium content, nor in the frequency of VEBs. After the magnesium infusions, however, a significant increase was noted in the cellular potassium content and likewise a significant decrease in the frequency of VEBs. This emphasizes the importance of magnesium in potassium metabolism.

Relationship between cellular electrolytes and the contraction force of isolated guinea-pig atria with special regard to the extracellular space volume

A micromethod is described which allows the quantitative evaluation of the extracellular space volume of isolated guinea-pig atria (> 15 mg tissue wet weight) by means of an enzymatic estimation of inulin. In addition, the acidic tissue extracts are analysed for the potassium, sodium, magnesium, calcium and 45calcium content. Taking into account the individual extracellular space volumes, it is possible to calculate the cellular electrolyte content and relative specific 45calcium activity of each atrium. Our experiments reveal under steady state conditions a significant correlation between the force of contraction and the cellular electrolyte content. Atria with a higher contraction force were found to contain a significantly elevated cellular potassium content and a lower content of cellular sodium and calcium than atria with a smaller contraction force. The decrease of cellular calcium content is exclusively caused by the lowering of the fraction of unexchanged tissue calcium. The significance of the results is discussed with respect to the events leading to contraction and relaxation of the heart muscle.