Potassium Influx Research Articles

Cation transport by modified dibenzo-18-crown-6 through lecithin liposomal membrane

Dibenzo-18-crown-6 was modified to a hydrophobic ionophore which was incorporated stably into a small unilamellar liposomal membrane of egg yolk lecithin. Vectorial sodium transport mediated by this ionophore through the membrane was measured directly by observing a 23Na NMR spectrometer. It was proposed that sodium efflux is balanced by potassium or lithium influx mediated by the ionophores through an ion-exchange mechanism.

Effect of glyburide on beta cell responsiveness to glucose in non-insulin-dependent diabetes mellitus

Since the introduction of glyburide in 1984, many studies have evaluated the effects of this oral hypoglycemic agent on beta cell function in patients with non-insulin-dependent diabetes mellitus. The early studies, which were performed in patients receiving concomitant insulin therapy, may have underestimated the true effect of glyburide on insulin secretion. The more recent studies demonstrate that both short- and long-term glyburide therapy increaes C-peotide levels in diabetic as well as nondiabetic subjects and that the effects of glyburide are comparable to those of the other second-generation sulfonylurea, glipizide. The effects of glyburide on insulin secretory rates calculated from plasma C-peptide levels were recently evaluated using individually derived C-peptide kinetic parameters and a validated open two-compartment model of peripheral C-peptide kinetics. Glyburide did not influence fasting insulin secretion (196 ± 34 versus 216 ± 23 pmol/min) but did cause an increase in the total amount of insulin secreted over a 24-hour period (447 ± 58 versus 561 ± 55 nmol). This increase in the production of insulin was generated by an increase in amplitude of secretory pulses occurring after lunch and dinner rather than by a greater number of pulses. The full effect of glyburide on the beta cell became evident when glucose concentrations were clamped at the hyperglycemic level of 300 mg/dL both befor and during treatment for a 3-hour period. During that time, insulin secretion rates increased by 221 percent in response to glyburide. Glyburide did not, however, completely reverse the beta cell secretory defect characteristic of non-insulin-dependent diabetes mellitus. In the patients receiving glyburide, the sluggish insulin secretory response to breakfast persisted, and the insulin secretory response during the hyperglycemic clamping was less than the response normally seen in nondiabetic subjects. These experiments suggest that the primary effect of glyburide on the beta cell is to increase its responsiveness to glucose. Although the precise mechanism of action of glyburide at the cellular level is unclear, in vitro studies suggest that its effect is mediated through binding with specific receptors on the beta cell membrane, which in turn leads to alterations in the cellular efflux of potassium ions and influx of calcium ions

Lymphocyte sodium pump numbers and potassium influx in pregnancy-induced hypertension

Lymphocyte sodium pump numbers and potassium influx in pregnancy-induced hypertension

Cation transport across lymphocyte plasma membranes in euthyroid and thyrotoxic men with and without hypokalaemic periodic paralysis

1. To study potassium transport in hypokalaemic periodic paralysis in a model of striated muscle cells, we measured specific [3H]ouabain binding (the number of sodium-potassium pumps), sodium-potassium-pump-mediated (ouabain-sensitive) 86Rb+ influx and sodium-potassium-pump-independent (ouabain-resistant) 86Rb+ influx in lymphocytes in vitro. 2. The subjects comprised euthyroid and thyrotoxic men with hypokalaemic periodic paralysis between attacks, men with uncomplicated thyrotoxicosis, and healthy men matched for age and weight. 3. Thyrotoxic patients, both with and without periodic paralysis, had significantly more lymphocyte sodium-potassium pumps than normal, and a significantly greater sodium-potassium-pump-mediated 86Rb+ influx. Anti-thyroid treatment corrected this defect in patients with thyrotoxic periodic paralysis. Euthyroid patients with cryptogenic periodic paralysis had significantly increased sodium-potassium-pump-mediated 86Rb+ influx, but a normal number of sodium-potassium pumps. 4. Only untreated thyrotoxic and euthyroid patients with periodic paralysis showed a significant increase in sodium-potassium-pump-independent 86Rb+ influx (5.2 +/- 2.8 and 4.5 +/- 1.8 respectively, vs control 2.8 +/- 1.0 pmol h-1 10(-6) cells; mean +/- SD; P less than 0.001, P less than 0.005). 5. We conclude that thyrotoxicosis increases the number and activity of sodium-potassium pumps and facilitates, but is probably not necessary for, periodic paralysis. Hypokalaemic periodic paralysis is associated with an increase in sodium-potassium-pump-independent potassium influx.

Influence of angiotensin converting enzyme inhibitor (captopril) on kidney epithelial cells in vitro: studies on potassium ( 86Rb) influx and cellular proliferation

The effects of captopril on potassium influx and cellular proliferation in a dog kidney epithelial cell line (Madin-Darby canine kidney cells, MDCK) were studied. Na +K +-ATPase activity and the loop diuretic sensitive Na/K/2Cl − cotransport were measured using 86Rb as tracer substance. Cells were incubated with various concentrations of captopril (1–10 mmol/l). The furosemide sensitive Na/K/2Cl − cotransport was significantly decreased from 1 mmol/l onwards. Na +/K +-ATPase activity was lowered only when high amounts (10 mmol/l) of the drug were used. Cell proliferation was measured via [ 3H]thymidine incorporation. After incubation with 1 mmol/l captopril proliferation was strongly decreased (> 50%). Higher amounts (5–10 mmol/l) did not further suppress cell proliferation. The data suggest that natriuresis following ACE inhibition in vivo does not involve a direct effect of captopril on Na +K +-ATPase. However, the effect on cell proliferation may be of clinical relevance in respect to a possible mitogenic effect of angiotensin II.

Potassium influx in human neonatal red blood cells. Partition into its major components

The potassium influx in human neonatal red blood cells (nRBC) shows an approximately 25% lower value compared to the total potassium influx in adult red blood cells (aRBC). The ouabain-sensitive potassium influx component represents approximately 70-75% of the total potassium influx for both types of cells but with an absolute value significantly lower in nRBC. In nRBC, the half maximum inhibitory effect for ouabain was obtained at a 10(-9) M concentration. The ouabain-insensitive nRBC potassium influx fractions showed two components: (i) a bumetanide-sensitive component, significantly lower than that of aRBC, (ii) a ouabain-bumetanide-insensitive (leak) component with a similar value in both cell types. The sum of the ouabain-sensitive and furosemide-sensitive components amounted in nRBC to a greater value than the total potassium influx. This behaviour could be interpreted as a superposition of the action of the inhibitors on the components affected.

A method for determining Michaelis‐Menten kinetic parameters of nutrient uptake for plants growing in soil

AbstractThe relationship between nutrient influx (In) and solution concentration at the root surface (Clo) has not yet been determined for roots growing in soil because of difficulties in measuring Clo. Corn was grown on two soils with 12 and 21% clay. Each soil had five K levels ranging from low to very high. Potassium influx (In) was determined from K uptake between two harvests and root length. Clo was then calculated from the average soil solution concentration and In by assuming that diffusion is the main transport mechanism for K to the root. Potassium influx plotted against Clo showed a saturation curve, typical of a Michaelis‐Menten kinetic relationship. The Michaelis‐Menten uptake parameters, maximum influx (Imax) and Michaelis constant (Km), were obtained by the “Hanes” plot. There was close agreement, without lack of fit, between calculated and observed data. The proposed procedure therefore appears to be suitable for estimating the uptake kinetics of roots growing in soil. Requirements for applications of the method are discussed.

The Na+,K+,2Cl- -cotransport system in HeLa cells and HeLa cell mutants exhibiting an altered efflux pathway.

We have investigated the characteristics of a transport system in HeLa cells, which turned out to be very similar to a previously described Na+, K+, 2Cl- -cotransport system. For further understanding about the physiological role of the cotransporter, we have mutagenized HeLa cells and selected progeny cells for growth in low potassium (0.2 mM) medium. The selected HeLa cells (LK1) exhibited alterations in the Na+,K+,2Cl- -cotransport system. LK1 cells showed a remarkable reduction of 86Rb+ efflux via the cotransporter when compared to the parental HeLa cells. In contrast, bumetanide-sensitive potassium influx, measured by 86Rb+ uptake, was increased in the LK1 cells (increase in Vmax). Km values of the cotransporter in HeLa cells and LK1 mutants revealed similar properties for 86Rb+ and 22Na+ uptake. In addition, (3H)-bumetanide binding studies were carried out on intact HeLa cells; 1.7 pmol/mg protein (3H)-bumetanide was specifically bound to HeLa parental cells, which could be calculated to a number of 103,000 binding sites/cell. LK1 cells present, 1.44 pmol/mg protein, specifically bound (3H)-bumetanide and, respectively, 137,000 binding sites/cell. The LK1 cells also exhibited an increase in the number of (3H)-ouabain binding sites as well as an increase in the activity of the Na+,K+-ATPase, expressed as a function of ouabain-sensitive 86Rb+ uptake. Furthermore, LK1 cells were different in the concentrations of intracellular Na+ (increases) and K+ (decreases) when compared to the HeLa parental cells. When grown in low K+ medium (0.2 mM K+), protein content and cell volume were increased in the LK1 cells, while the DNA content was not significantly different between both cell lines.

86Rb(K) influx and [ 3H]ouabain binding by human platelets: Evidence for β-adrenergic stimulation of Na-K ATPase activity

Although active transport of potassium into human platelets has been demonstrated previously, there is hitherto no evidence that human platelets have an ouabain-inhibitable Na-K ATPase in their membrane. The present study demonstrates active rubidium (used as an index of potassium influx), 86Rb(K), influx into platelets, inhibitable by ouabain, and also demonstrates the presence of specific [ 3H]ouabain binding by the human platelet. This 86RB(K) influx was stimulated by adrenaline, isoprenaline, and salbutamol, but noradrenaline caused a mild inhibition. Active 86Rb(K) influx by platelets was inhibited markedly by timolol, mildly by atenolol, but not by phentolamine. Therefore, active 86Rb(K) influx in human platelets is enhanced by stimulation of β adrenoceptors of the β 2 subtype. The platelet may therefore replace the leukocyte in future studies of Na-K ATPase activity. This would be a considerable advantage in view of the ease and rapidity of preparation of platelets.

Effects of carbamylcholine and isoproterenol on electrolyte fluxes in perfused main duct of submandibular gland of reserpinized rat.

Administration of reserpine (RES) at a dosage of 0.5 mg/kg body wt, ip daily for 7 days was found to lower the dose of carbamylcholine and isoproterenol that alters sodium and potassium transport by cells of the main duct of rat submandibular gland. In the perfused main excretory duct of the submandibular gland of the RES rat, administration of carbamylcholine at a dosage of 1 microgram/kg body wt, inhibited net efflux of sodium (17%) and administration of isoproterenol at a dosage of 2 micrograms/kg body wt increased net efflux of sodium (20%); these drugs, at the same dosages, did not induce significant change in electrolyte flux of normal rat. At a dosage of 5 micrograms/kg body wt, carbamylcholine decreased net influx of potassium (15%) in the RES rat but was without effect on normal rat. Isoproterenol at the dosage of 5 micrograms/kg body wt significantly inhibited net influx of potassium in both the RES rat and normal rat. The data suggested that the duct cells developed supersensitivity to sympathomimetic and parasympathomimetic stimulation after chronic RES treatment.

A comparison of two methods for measuring potassium influx kinetics by intact corn seedlings1

Abstract Growth chamber studies were conducted to compare two procedures for measuring potassium influx kinetics by intact corn (Zea mays L.) seedlings. It was assumed in both procedures that K uptake by corn followed Michaelis‐Menten kinetics. In the first procedure (depletion method) corn seedlings were grown in complete nutrient solution for 7, 10, 14 and 28 days. The nutrient solution contained ≤ 500 μM K. Potassium influx kinetics were determined by transferring plants into nutrient solution containing 200 μM K and following the rate of K depletion from solution over time. In the second procedure (Hofstee method) six K concentrations ranging from 24 to 246 μM were established and maintained by daily additions of K. Corn seedlings were harvested from each of the six treatments at 7, 10, 14, 21 and 28 days and K was measured in the shoots and roots. Average net K influx rates were calculated for each treatment at each harvest date. The average influx rates were paired with the measured average K concen...

Volume-sensitive, Cl-dependent K transport in resealed human erythrocyte ghosts

Potassium influx and efflux in Cl and NO3 media were measured in resealed ghosts prepared from human red cells. Cl-dependent K influx was three times that in intact cells and, as in intact cells, was partially supported by Br but not by thiocyanate (SCN). In other properties, this flux differed from that in intact cells: substitution of N-methylglucamine for Na did not decrease but rather increased Cl-dependent K influx, the affinity for external K was reduced, with a Km of 21.3 +/- 12.5 mM, and inhibition by furosemide and bumetanide was incomplete. Furosemide at 1 mM inhibited Cl-dependent influx by 26 and 51% at 4 and 20 mM K, respectively. Bumetanide inhibited Cl-dependent K influx by 0 and 55% at concentrations of 10 microM and 1 mM, respectively, in 4 mM K, with no further inhibition at 20 mM K. Neither the magnitude nor the properties of the flux were altered by preparing ghosts in the presence of 1,4-dithiothreitol, indicating that sulfhydryl oxidation was not responsible for the altered flux in ghosts. Treatment with N-ethylmaleimide (NEM) either before or after ghost preparation did not increase Cl-dependent K influx. However, Cl-dependent influx in ghosts could be augmented by increasing ghost volume or ATP content. Resealed human erythrocyte ghosts thus exhibit a volume- and ATP-sensitive, Cl-dependent K flux that differs substantially from the putative Na-K-Cl cotransport in intact cells in that it is independent of Na, is relatively resistant to furosemide and bumetanide, and has a low affinity for K.(ABSTRACT TRUNCATED AT 250 WORDS)

Depression of Nitrate and Ammonium Transport in Barley Plants with Diminished Sulphate Status. Evidence of Co-regulation of Nitrogen and Sulphate Intake

When barley plants were grown in a solution with nitrate as the sole N-source but deprived of sulphate (−Splants) for 1 to 5 d, the capacity for sulphate transport by the roots increased very markedly; subsequent measurement of influx using 35S-labelled SO42- showed increases of > 10-fold compared to plants continuously supplied with sulphate (+S plants). There were only small effects on plant growth over a 5 d period and yet the influx of NO3-⁠, labelled with the short-lived tracer 13N, was diminished by approximately 30%. By contrast, the influx of phosphate was little affected by sulphate-deprivation. When a sulphate supply was restored to − S plants, the sulphate influx was quickly repressed over the subsequent 24 h and the nitrate influx was restored to >90% of the value in +S plants. When plants were grown in a solution with a mixed nitrate and ammonium supply and deprived of sulphate for 1 d or 5 d the depression of nitrate influx was more strongly marked (up to 55% depression). The influx of ammonium was also depressed after 5 d of sulphate-deprivation, but not at 1 d, nor where the concentration of ammonium in the uptake solution was lowered to 20 mmol m−3 or less. Additional measurements with 15N-labelled nitrate and ammonium over longer periods were used to determine net uptake. Net uptake of nitrate was depressed to a similar extent to efflux, but net ammonium uptake was depressed only in unbuffered uptake solution where the pH decreased to pH 4.9 during the uptake period. The 15N-tracer experiments showed that the translocation of label to the shoot, from both nitrate and ammonium, was depressed to a greater extent than net uptake in −S plants. The depression of nitrate influx, caused by 5 d of sulphate deprivation, could be relieved almost completely by providing plants with 1.0 mol m−3 L-methionine during the day prior to influx measurement. This treatment substantially decreased sulphate and potassium (86Rb-labelled) influx in both +S and −S plants, but greatly increased total S-status of the plants. This methionine treatment had no effect on ammonium influx or net uptake in − S plants but increased influx significantly in +S ones. When plants were grown with sulphate but deprived of nitrate for 4 d there was a marked depression of the sulphate influx (by 48–65%) but a smaller effect on phosphate influx (21–37% of +N). The results are discussed in relation to the effects of sulphate-deprivation on growth rate and the root: shoot weight ratio. It is concluded that the effects on influx and net uptake of nitrogen are more severe than could be accounted for by these factors. The decreased translocation of either nitrate, or the products of nitrate and ammonium assimilation from the roots, is suggested as a reason for the depression of influx. The restoration of nitrate influx and net uptake by methionine suggests that, for this ion at least, a shortage of S-amino acids within the plant may lead to the accumulation of inhibitory concentrations of non-S amino acids in the transport pool.

Nitrogen‐stimulated potassium influx into maize roots: differential response of components resistant and sensitive to ambient ammonium1

Abstract Potassium (86Rb) influx from 200 mmol m −3 KCl into dark grown, decapitated maize seedlings 6 d old) was stimulated by nitrate pretreatment. The stimulus was clearly evident by 6h exposure to nitrate and required 12–24 h for maximal expression. Decay of the nitrate‐stimulated potassium influx was more than 50% complete within 3 h after transfer to nitrogen‐free solutions. The stimulation of potassium influx was entirely accounted for by an increase in the influx component that was resistant to inhibition by presence of 200 mmol m−3 ambient ammonium. In contrast, the component of potassium influx that was sensitive to inhibition by ambient ammonium was unaffected by nitrate pretreatment. Exposure to the glutamine synthetase inhibitor L‐methionine‐dl‐sulphoximine (MSX) during nitrate pretreatment stimulated the resistant component but the sensitive component was nearly eliminated. Pretreatment with ammonium increased the resistant component of potassium influx within 3 h, i.e. before it was increased by nitrate pretreatment, but the sensitive component was concomitantly restricted. The latter recovered partially during extended pretreatment with ammonium. The data indicate that the resistant component responded positively to increases in tissue ammonium concentrations whereas the sensitive component was unaffected by tissue ammonium except at concentrations in excess of 10μmol g−1. Ammonium influx was also stimulated by nitrate pretreatment and to a greater extent than potassium influx. Presence of MSX with nitrate during pretreatment resulted in a further stimulation in ammonium influx. The parallel increases in root ammonium concentrations with the two pretreatments imply that part of the increase in ammonium influx was a consequnce of increased counter‐transport with endogenous ammonium.

Density-related changes of potassium (86Rb) uptake by amphibian endothelial cells.

Potassium influx has been investigated in XTH-2 cells, a line derived from tadpole heart endothelia. In this line, the density at which the cultures become confluent is clearly separated from the density at which growth arrest takes place. Density-related changes in K+ influx were monitored by determining the uptake of 86Rb into well adhering cells kept in culture medium. The main observations were 1) 86Rb uptake is highest in single cells, and on confluency it reaches a low level, which is kept constant at higher cell density regardless of whether the cultures are stationary or still in logarithmic growth phase; 2) the relative amount of 86Rb taken up via the Na+ -K+ -2Cl- cotransport pathway and via the Na+/K+ pump changes from low cell density to confluent cultures; 86Rb uptake of single cells is nearly insensitive to ouabain, a maximum of ouabain sensitivity is reached around confluency, whereas piretanide-sensitive 86Rb uptake is highest in single cells and seems to reach a minimum at the onset of confluency; 3) the variations in Na+/K+ pumping rate reflect neither differences in the amount of enzyme present nor changes in enzyme repartition between apical and basolateral plasma membranes; they seem to result from either "masking" or "unmasking" of the enzyme; 4) no alterations in K+ uptake occur that would be characteristic of the "stationary growth phase." The only changes that seem to be related to arrest of proliferation are concerned with the Na+/K+-ATPase, which achieves an extraordinary susceptibility to stimulation by monensin and exhibits an increase in PNPPase activity.

Effects of nonionic amphiphiles at sublytic concentrations on the erythrocyte membrane.

The interactions of octaethyleneglycol alkylethers (C10-C16), pentaethyleneglycol dodecylether, and dodecyl D-maltoside with the human erythrocyte membrane were studied. All the amphiphiles protected erythrocytes against hypotonic haemolysis. At concentrations where the amphiphiles protected erythrocytes against hypotonic haemolysis they reduced phosphate efflux. The potency of the amphiphiles, at equiprotecting concentrations, was correlated negatively to the length of the alkyl chain. Potassium fluxes were increased by all the amphiphiles at protective concentrations. The relative potency of the amphiphiles varied but it was not simply related to the length of the alkyl chain. The only amphiphile affecting active potassium influx was octaethyleneglycol decylether which induced a slight decrease. It is concluded that the increase in passive cation fluxes caused by the amphiphiles is due to an increased permeability of the lipid bilayer induced through a nonspecific interaction of the amphiphiles with the bilayer. The effect of the amphiphiles on ion transport mediated by membrane proteins is proposed to be due to an alteration of the state of the transporting protein.

Inhibition of ouabain-insensitive potassium influx by the potassium channel blockers tetraethylammonium and caesium : T.W. Smith, J.C. Ellory, T. Powell, V.W. Twist. University Laboratory of Physiology, Parks Road, Oxford OX1 3PT

Inhibition of ouabain-insensitive potassium influx by the potassium channel blockers tetraethylammonium and caesium : T.W. Smith, J.C. Ellory, T. Powell, V.W. Twist. University Laboratory of Physiology, Parks Road, Oxford OX1 3PT

Simultaneous influx of ammonium and potassium into maize roots: kinetics and interactions

The interaction between ammonium and potassium during influx was examined in roots of dark-grown decapitated corn seedlings (Zea mays L., cv. Pioneer 3369A). Influx was measured during a 10-min exposure to either ((15)NH4)2SO4 ranging from 10 to 200 μM NH 4 (+) with and without 200 μM K((86)Rb)Cl or to K((86)Rb)Cl ranging from 10 to 200 μM K(+) with and without 200 μM NH 4 (+) as ((15)NH4)2SO4. The simple Michaelis-Menten model described the data well only for potassium influx in the presence of ambient ammonium. For the other three instances, the data were improved by assuming that a second influx mechanism became operative as the low-concentration phase approached saturation. Two distinct mechanisms are thus indicated for both ammonium and potassium influx within the range of 10 to 200 μM.The influx mechanism operating at low concentrations showed greater affinity for potassium than for ammonium, even though the capacity for ammonium transport was twice as large as that for potassium. It is suggested that this phase involved a common transport system for the two ions and that localized low acidity next to the internal surface, following H(+) extrusion, favored ammonium deprotonation and dissociation from the transport system-ammonium complex. Parallel decreases in V max and increases in Km of the low-concentration saturable phase occurred for ammonium influx when ambient potassium was present and for potassium influx when ambient ammonium was present. The data support a mixed-type inhibition in each case. Simultaneous measurement of potassium and ammonium influx showed that they were highly negatively correlated at the lower concentrations, indicating that the extent to which influx of the inhibited ion was restricted was associated with influx of the inhibitor ion. Presence of ambient ammonium eliminated the second phase of potassium influx. In contrast, the presence of ambient potassium decreased the concentration at which the second phase of ammonium influx was initiated but did not restrict the rate.

Equatorial potassium currents in lenses

Earlier work with the vibrating probe demonstrated the existence of outward potassium currents at the equator and inward sodium currents at the optical poles of the lens. By adding microelectrodes to the system, it is possible to relate steady currents (J) to the potential difference (PD) measured with a microelectrode. By injecting an outward current (I), it is possible to determine resistances and also the PD at which the steady outward potassium current becomes zero (PDJ = 0). At this PD the concentration gradient for potassium efflux and the electrical gradient for potassium influx are balanced so that there is no net flow of potassium across the membranes associated with the production of J. The PDJ = 0 for 18 rat lenses was 86 mV and that for 12 frogs lenses was -95 mV. This agrees with the potassium equilibrium potential and provides strong evidence to support the view that the outward equatorial current, J, is a potassium current. With the injection of outward current, I, the PD becomes more negative, the outward equatorial current, J, decreases, and the inward current at the optical poles increases. This suggests that there are separate electrical loops for K+ and Na+ that are partially linked by the Na, K-pump. Using Ohm's law, it is possible to calculate the input resistance (R = delta PD/I), the resistance related to the production of J (RJ = delta PD/delta J), and the effect of the combined resistances (delta J/I). The driving force for J can be estimated (PDJ = 0-PD). The relationships among currents, voltages and resistance can be used to determine the characteristics of the membranes that are associated with the outward potassium current observed at the equator. The effects of graded deformation of the lens were determined. The effects were reversible. The sites of inward and outward currents were not altered. Following deformation, the equatorial current, J, increased, and the PD became less negative. The PDJ = 0 remains the same so the ratio of K+ concentrations across the membrane responsible for J is unchanged. Therefore, the decrease in PD is ascribed to an increase in Na+ permeance with a resultant increase in driving force accounting for the increase in J.

Hypokalemia and ventricular arrhythmias in acute myocardial infarction.

In the present study, 408 patients with acute myocardial infarction were included. The serum concentration of potassium was assessed on admission. Episodes of ventricular fibrillation and/or ventricular tachycardia within the following 6 hours were registered. A significant positive correlation between hypokalemia and the incidence of malignant ventricular arrhythmias was demonstrated. Ongoing treatment with diuretics at the time of admission did not appear to be of any significance for the development of ventricular fibrillation or ventricular tachycardia. Out of 100 hypokalemic patients, only 33 were treated with diuretics. The main reason for hypokalemia in the early phase of an acute myocardial infarction is most likely an activation of the sympathetic nervous system leading to an influx of potassium from the extracellular to the intracellular body fluid compartment.