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PubMedDate not supplied

A single blind normal volunteer bioavailability study of a new microencapsulated potassium chloride tablet compared with two reference potassium formulations.

A single blind placebo controlled, cross-over study comparing a new microencapsulated potassium chloride tablet (MET) with two reference formulations of oral potassium, potassium chloride solution (PS) and potassium chloride wax-matrix tablets (WMT), was performed in 12 normal healthy volunteers. Urinary potassium excretion was the main criterion of comparison. Results showed that all three formulations have excellent bioavailability. This indicates that potassium absorption in the stomach is similar to that in more distant portions of the gut. The slow-release characteristics of both MET and WMT were confirmed. Clinical and pharmacological tolerance was excellent and no side-effects were reported with any of the potassium formulations studied.

Administration, Oral↗
PubMed1976

Influence of severe potassium depletion and subsequent repletion with potassium on muscle electrolytes, metabolites and amino acids in man.

1. Two women with severe hypokalaemic alkalosis were investigated by means of muscle biopsy before and at the end of 2 and 3 weeks respectively of intense therapy with potassium chloride. 2. The muscle biopsy material was analysed for water, electrolytes, adenine nucleotides, phosphocreatine, free creatine, pyruvate, lactate, glycogen and free amino acids. The extra- and intra-cellular distribution of water, electrolytes and amino acids was calculated by the chloride method. 3. Both patients showed a marked loss of intracellular potassium and an increase in intracellular sodium concentration. The muscle magnesium content was also slightly decreased. After repletion with potassium chloride, muscle sodium and potassium became normal. 4. The contents of creatine phosphate, ATP, ADP, AMP, lactate and pyruvate were within normal limits, but the phosphocreatine/total creatine ratio was reduced. After repletion, a small change in the apparent creatine-phosphokinase equilibrium had occurred, suggesting a minor increase in intracellular pH. 5. The concentrations of the basic amino acids, lysine, arginine and ornithine were increased far above normal. The intracellular accumulation of arginine was much higher than the increase in lysine concentration and histidine concentration was normal. This differs from findings in potassium-depleted rats, where the intracellular lysine concentration is much higher than arginine concentration and histidine is high as well. After potassium repletion the intracellular concentration of ornithine, lysine and arginine became normal in one case and decreased considerable in the other. An increased intracellular concentration of glutamate and glutamine was also observed after potassium repletion.

Acidosis↗
PubMed1967

Tracer and nontracer potassium fluxes in squid giant axons and the effects of changes in external potassium concentration and membrane potential.

The efflux of labeled and unlabeled potassium ions from the squid giant axon has been measured under a variety of experimental conditions. Axons soaked in sea water containing 42K ions lost radioactivity when placed in inactive sea water according to kinetics which indicate the presence of at least two cellular compartments. A rapidly equilibrating superficial compartment, probably the Schwann cell, was observed to elevate the specific activity of 42K lost from such axons to K-free sea water for a period of hours. The extra radioactive potassium loss from such axons during stimulation, however, was shown to have a specific activity identical within error to that measured in the axoplasm at the end of the experiment. The same was shown for the extra potassium loss occurring during passage of a steady depolarizing current. Axons placed in sea water with an elevated potassium ion concentration (50 mM) showed an increased potassium efflux that was in general agreement with the accompanying increase in membrane conductance. The efflux of potassium ions observed in 50 mM K sea water at different membrane potentials did not support the theory that the potassium fluxes obey the independence principle.

Action Potentials↗
PubMed1993

Oral magnesium supplementation restores the concentrations of magnesium, potassium and sodium-potassium pumps in skeletal muscle of patients receiving diuretic treatment.

In 76 consecutive patients who had received diuretics for 1-17 years for arterial hypertension or congestive heart failure, muscle concentrations of magnesium, potassium, and sodium-potassium pumps were significantly reduced compared to 31 age- and sex-matched controls. Thirty-six patients with muscle magnesium and/or potassium below the control level received oral magnesium hydroxide supplement for 2-12 weeks (n = 20) or 26 weeks (n = 16). After short-term (2-12 weeks) magnesium supplementation muscle parameters were increased, but far from normalized. After magnesium supplementation for 26 weeks, the muscle concentrations of magnesium, potassium and sodium-potassium pumps were normalized in most cases. Oral magnesium supplementation may restore diuretic-induced disturbances in the concentrations of magnesium, potassium and sodium potassium pumps in skeletal muscle. A supplemental period of at least 6 months seems to be required before complete normalization can be expected.

Administration, Oral↗
PubMed1990

Three different potassium channels in human atrium. Contribution to the basal potassium conductance.

We applied the cell-attached and inside-out patch-clamp technique under symmetrical isotonic potassium conditions on single human (and guinea pig) atrial cells. The human cells were isolated by a modified method to that described earlier. Our aim was twofold: 1) to study the single-channel characteristics of potassium channels in human atrial single cells, present under basal conditions (iK1 and iK(ATP] or when stimulated with 10(-5) M acetylcholine; and 2) to calculate the contribution of these three channel types to the total basal potassium conductance in human atrial cells, and to compare the results with data on guinea pig atrial cells under the same conditions. We found that in human cells 58% of the patches (n = 42/74) contained acetylcholine-sensitive potassium channels: their conductance was 42 +/- 1.2 pS and mean open time (tau o) was 1.7 +/- 0.5 msec. They showed sporadic openings in the absence of agonist, and activation by acetylcholine was G-protein dependent. In 16% of the patches (n = 7/44), adenosine (10(-4) M) activated the same channels, but the activity was lower than when stimulated by acetylcholine. In 18% of the patches (n = 9/51), an iK1 channel was present (conductance, 27 pS; tau o, 8.7 msec), whereas in the cell-attached mode, ATP-dependent channels were never seen. However, they were present in half of the inside-out patches on washout of ATPi (conductance, 73 pS; tau o, 1.4 msec). The basal potassium conductance (i.e., in the absence of any exogenous hormone or neurotransmitter) was mainly due to iK1 channels in both human and guinea pig cells, a finding that is in contrast with previous reports. However, the potassium current that is induced by acetylcholine is much higher in guinea pig than in human isolated cells; a fraction of it would suffice to fully determine the resting potassium conductance in guinea pig atrial cells, whereas it can play only a modulatory role in human cells. This difference could be important in species-specific autonomic modulation and antiarrhythmic drug action.

Acetylcholine↗
PubMed1973

The role of Na-K-activated adenosine triphosphatase in potassium adaptation. Stimulation of enzymatic activity by potassium loading.

The specific activity of sodium-potassium-activated adenosine triphosphatase (Na-K-ATPase) in homogenates of rat kidneys increases when the dietary intake of potassium is chronically increased. The effect is seen first and is most prominent in the outer medulla, but large loads of potassium elicit an increase in the cortex as well. Levels of Na-K-ATPase in brian, liver, and muscle, by contrast, are unaffected by potassium loading. Although the changes in enzyme activity in the kidney resemble those reportedly produced by aldosterone, they are not induced by experimental sodium deprivation, and they can be evoked by potassium loading in the absence of the adrenal glands. The results suggest that Na-K-ATPase of renal tubular cells, presumably in the distal tubules and collecting ducts, plays an important role in the phenomenon of potassium adaptation and in the process by which potassium is excreted into the urine.

Adaptation, Physiological↗
PubMedDate not supplied

[Comparative evaluation of the toxicity of potassium hydrocarbonate and potassium chloride].

The potassium hydrocarbonate and potassium chloride toxicity was compared in experiments on 113 albino rats. The death following introduction of maximal amounts of potassium chloride was noted to supervene earlier than it did in animals receiving equivalent doses of potassium hydrocarbonate. Simultaneous introduction of sodium hydrocarbonate lowered the toxicity of both potassium hydrocarbonate and chloride. Morphological investigations revealed that toxic doses of potassium hydrocarbonate bring about shifts in the carbohydrate and lipids metabolism. Some mechanisms behind the action produced potassium chloride and hydrocarbonate are discussed.

Animals↗
PubMed1985

Potassium supplementation fails to lower blood pressure in hypertensive patients receiving a potassium losing diuretic.

Thirty-three patients with hypertension receiving drug treatment that included a potassium losing diuretic were randomly allocated to 64 mmol of potassium (14 patients) or to no additional potassium supplementation (19 patients). Potassium was administered as slow release potassium chloride. After 3 months, blood pressure fell by 5/1 mm Hg in the patients who received the supplements and by 7/4 mm Hg in those who did not receive them. The falls in pressure were not significantly different and the 90% confidence limits for the effect of supplementation on diastolic pressure were: a fall of 2 mm Hg and a rise of 11 mm Hg, thus excluding an important hypotensive effect in these patients. Conversely, plasma creatinine fell by 11% in the supplement group compared with a 6% rise in the control group (P less than 0.05). Potassium supplementation, either by pharmacological preparations or by dietary manipulation, may prove to be desirable in patients on a potassium losing diuretic but should not be expected to lower blood pressure in such patients.

Benzothiadiazines↗
PubMed1994

[Oral magnesium supplementation to patients receiving diuretics--normalization of magnesium, potassium and sodium, and potassium pumps in the skeletal muscles].

In 76 consecutive patients who had received diuretics for 1-17 years for arterial hypertension or congestive heart failure, muscle concentrations of magnesium, potassium, and sodium-potassium pumps were significantly reduced compared to 31 age- and sex-matched controls. Thirty-six patients with muscle magnesium and/or potassium below the control level received oral magnesium hydroxide supplement for 2-12 weeks (N = 20) or 26 weeks (N = 16). After short term (2-12 weeks) magnesium supplementation muscle parameters were increased, but far from normalized. After magnesium supplementation for 26 weeks, the muscle concentrations of magnesium, potassium and sodium-potassium pumps were normalized in most cases. Oral magnesium supplementation may restore diuretic-induced disturbances in the concentrations of magnesium, potassium and sodium-potassium pumps in skeletal muscle. A supplemental period of at least six months seems required before complete normalization can be expected.

Administration, Oral↗
PubMed1995

Total body potassium and serum potassium among eating disorder patients.

OBJECTIVE: The purpose of the study was to determine body composition, including total body potassium (TBK+), serum potassium, and lean body mass (LBM), in anorexia nervosa. METHOD: TBK+ measurements, serum potassium levels, and anthropometric measurements were obtained from four anorectic patients in the first week after their hospital admission. All four patients had normal serum potassium levels but three of the four had significant depletion of total body potassium. Two methods of calculating LBM, based on TBK+ measures or anthropometric assessment, produced different results. RESULTS: TBK+ may be depleted even when serum potassium levels are normal. It was also concluded that the two methods of calculating LBM were inaccurate. DISCUSSION: Patients may be at risk for cardiac arrhythmias and other physiological abnormalities even when serum potassium is normal since TBK+ may be low. The need for comprehensive assessment of body composition based on four compartment models is discussed.

Adult↗
PubMed1990

Effects of potassium channel openers on single potassium channels in mouse skeletal muscle.

The patch-clamp technique was used to study the effects of the potassium channel openers cromakalim, pinacidil, RP 49356 and diazoxide on single potassium channels in mouse skeletal muscle. In excised patches in the inside-out configuration, one type of potassium channel, the ATP-sensitive potassium channel, could be activated by internally applied RP 49356 even in the absence of internal ATP. At a concentration of 0.4 and 0.8 mmol/l, RP 49356 increased the open-probability of the channels by a factor of 2.7 and 17.4 respectively. The stimulating effect of cromakalim (0.2-0.8 mmol/l) and pinacidil (0.4 mmol/l) depended on the presence of ATP (0.1 mmol/l) at the cytoplasmic side of the patch membrane. The two drugs were able to restore the open-probability of the channels blocked by internal ATP (0.1 mmol/l) to 50-90% of its value in ATP-free solution. No channel reactivation could be observed at a higher ATP concentration (1 mmol/l). Diazoxide (0.4 mmol/l) had almost no effect. None of these channel openers could stimulate the other prominent type of potassium channel in skeletal muscle, the large-conductance Ca2(+)-activated potassium channel. The results show that cromakalim, pinacidil and RP 49356 are specific openers of ATP-sensitive potassium channels in skeletal muscle. It is suggested that the drugs displace the channel blocker ATP and that RP 49356 in addition recruits inactive channels.

Adenosine Triphosphate↗
PubMed1982

Relation of arterial pressure with body sodium, body potassium and plasma potassium in essential hypertension.

1. Exchangeable sodium (NaE), plasma electrolytes and arterial pressure were measured in 121 normal subjects and 91 patients with untreated essential hypertension (diastolic greater than 100 mmHg), 21 of whom had low-renin hypertension. Plasma concentrations of renin, angiotensin II and aldosterone were measured in all hypertensive patients, total body sodium, total body potassium and exchangeable potassium (KE) in some patients. 2. Mean NaE was not different in normal and hypertensive subjects provided the two groups were matched for leanness index. In the subgroup of young hypertensive patients aged 35 years or less mean NaE was below normal. NaE was not related to arterial pressure in normal subjects but in hypertensive patients there were positive and significant correlations of arterial pressure with NaE and with total body sodium. 3. NaE and total body sodium increased with age in hypertensive but not in normal subjects. Partial regression analysis suggested that the correlation of NaE with arterial pressure was not explained by an influence of age. 4. Mean NaE was not increased and mean KE was not decreased in patients with low-renin hypertension. 5. Plasma potassium concentration, KE and total body potassium correlated inversely and significantly with blood pressure in hypertensive patients. These correlations were more marked in young than in old patients. 6. Multiple regression analysis showed that the combination of NaE and plasma potassium concentration 'explained' more of the variation of systolic blood pressure in hypertensive patients than it did in normal subjects. Plasma potassium concentration 'explained' more of the variation in young hypertensives and NaE 'explained' more in older patients. 7. Our findings suggest than changes of plasma and body potassium are important in the earlier stages of essential hypertension and that changes of body sodium become important later.

Adult↗
PubMed1987

The natriuretic effect of an acute peroral load of potassium chloride after inhibition of potassium secretion with amiloride or lithium.

The ability of the kidneys to excrete potassium after an acute peroral potassium load was studied in rats in which the kidney function was influenced by administration of amiloride or lithium for one month. Water, potassium chloride, or sodium chloride solutions were given by gastric tube immediately before a 2-hour clearance period. The results showed that a load of potassium given by gastric tube leads to an increase of potassium excretion in rats given either no treatment, amiloride, or lithium but the increase was about 50% lower in the lithium group. KCl administration provoked a considerable increase of sodium clearance (CNa) compared with the increase of CNa in the control group. The exaggerated natriuresis was apparently specific for potassium, since a peroral load of sodium chloride led to a more modest increase of CNa, an increase which was significant in control rats only. The increase of CNa in rats given a peroral load of potassium could not be explained by an increase of the proximal tubular fluid output, since the latter as measured by lithium clearance (CLi) remained unaltered. Since CNa/CLi rose considerably, the effect could be ascribed to an inhibition of the fractional distal sodium reabsorption.

Administration, Oral↗
PubMed1985

Can potassium citrate replace sodium bicarbonate and potassium chloride of oral rehydration solution?

Ninety four children aged less than 5 years with diarrhoeal dehydration and acidosis were treated randomly with either World Health Organisation (WHO) oral rehydration solution containing sodium chloride, potassium chloride, sodium bicarbonate and glucose or an oral solution with tripotassium citrate monohydrate replacing the sodium bicarbonate and potassium chloride in the WHO solution. Fifty five children (58%) were hypokalaemic (potassium less than 3.5 mmol/l) on admission. All but two in the citrate group were successfully treated. There were no significant differences in rehydration solution intake, stool output, gain in body weight, and fall in plasma specific gravity and haematocrit between the two treatment groups after 48 hours' treatment. Significant improvement in the serum potassium concentration was observed in the hypokalaemic children receiving potassium citrate solution compared with children receiving WHO solution after 24 and 48 hours' treatment. None developed hyperkalaemia. Although children receiving potassium citrate solution corrected their acidosis at a slower rate than the WHO solution group during the first 24 hours, by 48 hours satisfactory correction was observed in all. Tripotassium citrate can safely replace sodium bicarbonate and potassium chloride and may be the most useful and beneficial treatment for diarrhoea and associated hypokalaemia.

Acidosis↗
PubMed1981

Effect of potassium removal during hemodialysis on the plasma potassium concentration.

The effect of potassium removal by hemodialysis on the plasma potassium concentration (PK) was observed during 20 studies on 7 anuric patients. The following was observed: (1) The pattern of change in PK is consistent with at least a two-compartment distribution; hence, in contrast to urea, PK shows a marked postdialytic rebound and the simple equation for solute removal from a single pool cannot predict postdialysis PK. (2) The magnitude of the fall in PK correlated with the predialysis PK; this was not only due to increased potassium removal, but also due to a dependence of the apparent volume of distribution of potassium on the state of potassium balance. The fractional decrement in plasma potassium concentration, contrary to that of urea, is a function of predialysis concentration, and prediction of the effect of dialysis on plasma potassium concentration can assume neither a single pool nor a constant distribution volume for this ion.

Blood Urea Nitrogen↗
PubMed1990

Total body potassium, skeletal muscle potassium and magnesium in patients with Bartter's syndrome.

In 20 patients with Bartter's syndrome, who had a serum potassium concentration of 2.75 +/- 0.29 mmol/l (mean +/- SD), the total body potassium (TBK) was measured and compared with a predicted value obtained from regression equations based on age, sex, body height and weight. A significant difference was found between the observed and predicted TBK (mean -320 +/- 306 mmol, p less than 0.01). A positive correlation existed between the serum potassium concentration and the ratio observed TBK/predicted TBK. However, the average fractional reduction in TBK (-11%) was less than the average fractional decrease in serum potassium concentration (-32%). Muscle biopsy specimens were obtained from four patients with Bartter's syndrome and 10 control subjects for analyses of potassium and magnesium. The serum concentrations of potassium and magnesium were decreased in these patients. The potassium content in muscle tissue was lower in two of four patients, but no difference in the amount of magnesium was observed.

Adult↗
PubMed2003

Final report on the safety assessment of sodium sulfite, potassium sulfite, ammonium sulfite, sodium bisulfite, ammonium bisulfite, sodium metabisulfite and potassium metabisulfite.

Sodium Sulfite, Ammonium Sulfite, Sodium Bisulfite, Potassium Bisulfite, Ammonium Bisulfite, Sodium Metabisulfite, and Potassium Metabisulfite are inorganic salts that function as reducing agents in cosmetic formulations. All except Sodium Metabisulfite also function as hair-waving/straightening agents. In addition, Sodium Sulfite, Potassium Sulfite, Sodium Bisulfite, and Sodium Metabisulfite function as antioxidants. Although Ammonium Sulfite is not in current use, the others are widely used in hair care products. Sulfites that enter mammals via ingestion, inhalation, or injection are metabolized by sulfite oxidase to sulfate. In oral-dose animal toxicity studies, hyperplastic changes in the gastric mucosa were the most common findings at high doses. Ammonium Sulfite aerosol had an acute LC(50) of >400 mg/m(3) in guinea pigs. A single exposure to low concentrations of a Sodium Sulfite fine aerosol produced dose-related changes in the lung capacity parameters of guinea pigs. A 3-day exposure of rats to a Sodium Sulfite fine aerosol produced mild pulmonary edema and irritation of the tracheal epithelium. Severe epithelial changes were observed in dogs exposed for 290 days to 1 mg/m(3) of a Sodium Metabisulfite fine aerosol. These fine aerosols contained fine respirable particle sizes that are not found in cosmetic aerosols or pump sprays. None of the cosmetic product types, however, in which these ingredients are used are aerosolized. Sodium Bisulfite (tested at 38%) and Sodium Metabisulfite (undiluted) were not irritants to rabbits following occlusive exposures. Sodium Metabisulfite (tested at 50%) was irritating to guinea pigs following repeated exposure. In rats, Sodium Sulfite heptahydrate at large doses (up to 3.3 g/kg) produced fetal toxicity but not teratogenicity. Sodium Bisulfite, Sodium Metabisulfite, and Potassium Metabisulfite were not teratogenic for mice, rats, hamsters, or rabbits at doses up to 160 mg/kg. Generally, Sodium Sulfite, Sodium Metabisulfite, and Potassium Metabisulfite were negative in mutagenicity studies. Sodium Bisulfite produced both positive and negative results. Clinical oral and ocular-exposure studies reported no adverse effects. Sodium Sulfite was not irritating or sensitizing in clinical tests. These ingredients, however, may produce positive reactions in dermatologic patients under patch test. In evaluating the positive genotoxicity data found with Sodium Bisulfite, the equilibrium chemistry of sulfurous acid, sulfur dioxide, bisulfite, sulfite, and metabisulfite was considered. This information, however, suggests that some bisulfite may have been present in genotoxicity tests involving the other ingredients and vice versa. On that basis, the genotoxicity data did not give a clear, consistent picture. In cosmetics, however, the bisulfite form is used at very low concentrations (0.03% to 0.7%) in most products except wave sets. In wave sets, the pH ranges from 8 to 9 where the sulfite form would predominate. Skin penetration would be low due to the highly charged nature of these particles and any sulfite that did penetrate would be converted to sulfate by the enzyme sulfate oxidase. As used in cosmetics, therefore, these ingredients would not present a genotoxicity risk. The Cosmetic Ingredient Review Expert Panel concluded that Sodium Sulfite, Potassium Sulfite, Ammonium Sulfite, Sodium Bisulfite, Ammonium Bisulfite, Sodium Metabisulfite, and Potassium Metabisulfite are safe as used in cosmetic formulations.

Animals↗
PubMed1951

Cation exchange between cells and plasma of mammalian blood. II. Sodium and potassium exchange in the sheep, dog, cow, and man and the effect of varying the plasma potassium concentration.

Sodium and potassium exchange has been studied in the blood of the sheep, dog, cow, and man. The potassium exchange rate in human cells is practically unaltered by increasing the plasma potassium concentration approximately threefold. Comparing the results in different species the exchange rate for potassium shows a rough correlation with the intracellular amount of the element. Expressed in per cent of the cellular content sodium tends to exchange more rapidly than potassium. In three instances the specific activity curves deviate from the simple exponential behavior of a two compartment system. In the exchange of potassium in canine blood the deviation is caused by the presence of a rapidly exchanging fraction in the buffy coat cells. Such an effect does not account for the inhomogeneity of sodium exchange in human blood.

Animals↗