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PubMed1981

Hypokalemia--clinical spectrum and etiology.

This paper is intended to give a review of the etiology and symptoms of potassium deficiency in man, as an introduction to the section on potassium and cardiac arrhythmias of this symposium. A review is given of different conditions where hypokalemia and/or total potassium deficiency is or might be part of the clinical picture, such as conditions with insufficient dietary intake, gastrointestinal potassium losses (e.g. vomiting, fistulas, malabsorption, abuse of laxatives and diarrhea), and renal potassium losses (e.g. primary and secondary hyperaldosteronism, Cushing's syndrome, intake of licorice, diabetic coma, renal disease, diuretic treatment and l-dopa treatment). Common symptoms of hypokalemia and/or potassium deficiency are reviewed as well, such as general and unspecific symptoms (e.g. tiredness, lack of concentration, lack of appetite and vomiting), and symptoms from the heart, kidneys and skeletal muscle.

Diet↗
PubMed1987

Aldosterone biosynthesis and cytochrome P-45011 beta: evidence for two different forms of the enzyme in rats.

Whereas cytochrome P-45011 beta has been recently shown to catalyze the two-step conversion of corticosterone to aldosterone in the bovine and porcine adrenal cortex, the identity of the enzyme involved in the two final steps of aldosterone biosynthesis in the rat adrenal cortex is as yet unknown. Mitochondria from capsular adrenals of sodium-deficient, potassium-replete rats converted corticosterone to 18-hydroxycorticosterone and aldosterone at markedly higher rates than mitochondria from capsular adrenals of sodium-replete, potassium-deficient rats. However, the same preparations exhibited no difference in the 11 beta-hydroxylase activity, i.e. the conversion of deoxycorticosterone to corticosterone. Only mitochondria of zona glomerulosa from rats with stimulated aldosterone biosynthesis contained a 49K protein which showed a strong cross-reactivity with a monoclonal antibody raised against purified bovine cytochrome P-45011 beta. By contrast, a crossreactive protein with a molecular weight of 51K was found in mitochondria of zona fasciculata and in mitochondria of zona glomerulosa from rats with a suppressed aldosterone biosynthesis. These findings indicate the existence of two different forms of cytochrome P-45011 beta in the rat adrenal cortex, with only one of them, i.e. the 49K form, being capable of catalyzing the two final steps of aldosterone biosynthesis in situ.

18-Hydroxycorticosterone↗
PubMed1996

Protective action of isoquinolinesulfonamides in in vitro models of neuronal apoptosis.

We have previously reported that a group of isoquinolinesulfonamide kinase inhibitors (H7, 1-(5-isoquinolinesulfonyl)-2-methylpiperazine; H8, N-[2-(methylamino)ethyl]-5-isoquinolinesulfonamide; and H9, N-2-(aminoethyl)-5-isoquinolinesulfonamide) prevents apoptosis triggered in neurons by an inhibition of phosphatases 1 and 2A with okadaic acid, and by inhibition of protein kinase C with staurosporine and chelerythrine. In the present study we assessed the capability of isoquinolinesulfonamides (IQS) to prevent different types of apoptosis in primary cultures of cerebellar granule neurons. We induced apoptosis by: a) serum removal, b) potassium deficiency, c) serum removal + potassium deficiency, and d) beta-amyloid peptide (beta AP). The IQS prevented apoptosis in all the above models. Thus, it appears that the IQS-sensitive pathway is a common mechanism in different types of neuronal apoptosis, and that it might be used as a target in the development of novel neuroprotective drugs.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMedDate not supplied

[Potassium metabolism in diabetes mellitus].

A method of radiometry of the whole body in the low-background chamber was applied to the study of the content of total potassium (by K40) in the organism of 67 patients suffering from diabetes mellitus of various severity and in 76 healthy individuals. there was revealed a marked reduction of the total potassium level in diabetics. The more severe the diabetes--the greater the potassium deficiency. Total potassium level had a tendency to normalization after treatment with insulin, potassium salts and vitamins.

Adult↗
PubMed1998

Reappraisal of the quantity and nature of renal calcifications and mineral metabolism in the magnesium-deficient rat. Effects of treatment with potassium citrate or the combination magnesium citrate and potassium citrate.

There is an urgent need for drugs capable of inhibiting renal calcifications, nephrocalcinosis and stones included, in humans. Current anticalcification medication is based mainly on alkalinization of the metabolism using potassium-containing citrate alone, despite the fact that calcium stone patients suffer marginally from both magnesium and potassium deficiency. We investigated the anticalcification efficacy of oral potassium citrate versus the combined administration of this drug and magnesium citrate in the magnesium-deficient rat developing corticomedullary nephrocalcinosis and luminal microliths in the long term. Among other things we employed specific stains for calcium and oxalate, light microscopy and element analysis for renal tissue and calcifications, respectively. In addition, minerals in renal tissue, urine and plasma were determined, as well as the state of extracellular calcium homeostasis. Magnesium deficiency caused pure calcium phosphate tissue deposits, containing no magnesium, but no deposition of calcium oxalate in the tubular lumen; tissue magnesium, calcium and phosphorus were increased, and there was marked potassium wastage via urine; despite mild hypercalcemia other signs of hyperparathyroidism were not found. Alkalinization with the two kinds of medication evoked an increase in urinary pH, citrate, and potassium; however, potassium citrate alone tended to aggravate renal concretions, whereas the combination of this drug with magnesium citrate completely prevented concretions. It was concluded that: (1) magnesium deficiency-induced calcifications are oxalate-free and are not sensitive to mobilization by alkalinization with potassium citrate, which might explain the failure of the drug to prevent stone recurrence in clinical stone patients, and (2) the combination of potassium citrate and magnesium citrate, which shows enormous anticalcification efficacy, deserves high priority in clinical trials aimed at evaluating strategies for the prevention of stones.

Animals↗
PubMed1979

Mechanism of renal potassium conservation in the rat.

The mechanisms responsible for renal potassium (K) conservation during dietary potassium deficiency are poorly understood. This study was undertaken to investigate the time course of potassium conservation as well as the roles of distal sodium (Na) delivery, the distal delivery or sodium plus a nonpermeable anion, mineralocorticoid hormone, renal tissue potassium content, and Na-K-ATPase activity in renal potassium conservation. After 72 hours of a low-potassium diet, basal potassium excretion was negligible. After 24 hours, and even more so after 72 hours of potassium restriction, the kaliuretic response to increasing distal delivery of sodium or sodium plus a nonpermeable anion was impaired. After 24 hours of a low-potassium diet, plasma aldosterone levels fell from 180 +/- 25 to 32 +/- 9 pg/ml (P less than 0.001). Mineralocorticoid hormone given in the first 24 hours of a low-potassium diet resulted in a greater potassium loss (1564 +/- 125 muEq) than it did in controls on the same diet not receiving mineralocorticoid hormone (1032 +/- 83 muEq, P less than 0.005). In contrast, after 72 hours of diet, large doses of mineralocorticoid hormone failed to cause a kaliuresis in either anesthetized or conscious rats. After both 24 and 72 hours, outer medullary Na-K-ATPase was increased. At 72 hours, cortical, medullary, and papillary tissue potassium concentrations were significantly depressed. Acute administration of potassium repleted tissue potassium levels and restored basal and saline-stimulated potassium excretion to normal. Although potassium excretion was markedly depressed after 24 hours of the low-potassium diet, 42K microinjection studies of the distal nephron did not suggest any increase in potassium reabsorption. Following 72 hours of diet, potassium reabsorption increased significantly from 26 +/- 2% to 41 +/- 2% (P less than 0.001). We conclude that renal potassium conservation is at first primarily related to a decrease in potassium secretion, which is most likely mediated by falling levels of mineralocorticoid hormone. After 72 hours of the potassium-deficient diet, however, potassium conservation becomes independent of mineralocorticoid hormone, distal delivery of sodium, and Na-K-ATPase. The decreased tissue potassium content appears to be the primary mediator of both the increase in potassium reabsorption by the distal nephron and of renal potassium conservation at this time.

Aldosterone↗
PubMed1984

Sodium depletion of rats induces a mitochondrial protein in the zona glomerulosa of the adrenal cortex.

Sodium restriction of rats resulted in a marked increase in the concentration of a mitochondrial protein with a mol. wt of 49000 in the zona glomerulosa of the adrenal cortex. The same protein had been previously induced in potassium deficient rats by potassium repletion. Since both sodium depletion and potassium repletion are known to stimulate the activity of the mitochondrial mixed function oxidase involved in the conversion of corticosterone to aldosterone, the present observation supports the hypothesis that the potassium-induced protein might represent cytochrome P-450CMO (corticosterone methyl oxidase).

Adrenal Cortex↗
PubMed1970

The effect of uncomplicated potassium depletion on urine acidification.

Studies were performed on normal human subjects to determine the effects of potassium depletion on urine acidification. Depletion was induced by ingestion of a low potassium diet either alone or in combination with a potassium-binding resin, and the response of each subject to an acute ammonium chloride load in the potassium-depleted state was compared to his normal response. Urine pH was significantly higher during potassium deficiency if sufficient potassium depletion had been induced. No differences in blood acid-base parameters, urinary flow rate, or urinary fixed buffer excretion rate were found to account for this change; however, the increase in urine pH was accompanied by a concomitant increase in net acid and ammonium excretion. It is proposed that these changes during potassium depletion reflect an increase in ammonia diffusion into the urine, presumably as a result of increased renal ammonia production. In addition, it is speculated that changes in ammonia metabolism may be a physiologic control mechanism for potassium conservation.

Acid-Base Equilibrium↗
PubMed1987

Hypokalemic nephropathy in the rat. Role of ammonia in chronic tubular injury.

Chronic potassium deficiency results in progressive tubulointerstitial injury, associated with augmented renal ammoniagenesis. We investigated the role of elevated renal ammonia levels and the interaction of ammonia with the complement system in this injury. Potassium deficiency was induced in rats by feeding a low potassium diet. Experimental animals received 150 mM NaHCO3 or equimolar NaCl, as drinking water. After 3 wk, NaHCO3 supplemented rats demonstrated decreased ammonia production, less renal hypertrophy, less histologic evidence of injury, and less proteinuria. In in vitro studies on normal cortical tubular fragments, the addition of ammonia to serum in concentrations comparable to renal cortical levels in potassium-deficient animals significantly increased tubular deposition of C3 as quantitated by a radiolabeled antibody binding technique. Thus, alkali supplementation reduced chronic tubulointerstitial disease in a rat model of hypokalemic nephropathy. We propose that increased cortical ammonia levels contribute to hypokalemic nephropathy through ammonia-mediated activation of the alternative complement pathway.

Ammonia↗
PubMed1997

Relationship between turnover of cesium-137 and dietary potassium content in potassium-restricted mice.

The biological half-life of 137Cs and its organ distribution were investigated in mice fed various potassium-deficient diets. The biological half-life, which was 6.1 days in mice receiving the normal level of potassium, became longer as the dietary potassium content decreased, and 137Cs was hardly excreted from the body when dietary potassium content was restricted to 200 mg/kg or less. The muscle showed the highest concentration of 137Cs in both mice that had sufficient amounts of potassium and those that were potassium-deficient. Clearance of 137Cs from tissues was generally suppressed when mice were fed a potassium-deficient diet, but the relative distribution pattern of 137Cs was not affected by dietary potassium content. These results suggest that dietary potassium intake, which may vary with eating habits, affects the biological half-life of 137Cs in humans.

Animals↗
PubMed1988

Reduced concentrations of potassium, magnesium, and sodium-potassium pumps in human skeletal muscle during treatment with diuretics.

Animal studies have shown that potassium depletion induced by diuretics or potassium deficient fodder leads to a selective decrease in the concentrations of potassium and in the concentration of sodium-potassium pumps in skeletal muscle. In 25 patients who had received diuretics for 2-14 years the mean concentrations of potassium, magnesium, and sodium-potassium pumps were measured in skeletal muscle biopsy specimens and were significantly lower than in those from a group of age matched controls. The reductions in all three variables were significant in those patients receiving diuretics for arterial hypertension as well as in those being treated for congestive heart failure. In 14 patients the mean muscle potassium concentration was below the control range, but only one of those was hypokalaemic (3.4 mmol/l), and 13 were receiving potassium supplements. In 15 patients the mean muscle magnesium concentration was below normal, and the mean muscle potassium and magnesium concentrations showed a linear correlation. In 12 patients in whom the mean muscle potassium concentration was below 80 mumol/g wet weight there was a linear correlation between the cellular potassium:sodium ratio and the concentration of 3H-ouabain binding sites indicating that potassium deficiency also leads to a down regulation of sodium-potassium pumps in human skeletal muscle. In spite of potassium supplements long term treatment with diuretics may lead to potassium and magnesium deficiencies, which are not detectable using the standard methods of serum analysis. The changes in concentrations of electrolytes and sodium-potassium pumps associated with treatment with diuretics may impair muscle function and potassium homoeostasis and interfere with the distribution of digitalis glycosides.

Adult↗
PubMed1976

Effects of chlorthalidone on serum and total body potassium in hypertensive patients.

Total body potassium has been estimated in 26 hypertensive patients who were hypokalaemic as a result of long-term chlorthalidone treatment (mean 20.5 months), while they were on chlorthalidone and 4 weeks after this had been discontinued. The mean difference amounted to only 95 mEq (not significant). In 6 additional patients not previously treated with chlorthalidone, serial total body potassium estimations revealed a mean potassium deficiency of 245 mEq after 33 days and of 106 mEq after 100 days. These results suggest that the mechanism causing the initial potassium loss is partly reversed or compensated later on. In patients with uncomplicated hypertension, no significant potassium deficiency was detected during long-term treatment. Eighteen of our patients received 39 mEq potassium chloride supplements daily for 4 weeks; this caused a mean rise in serum potassium from 3.23 mEq/l to 3.38 mEq/l (not significant). Total body potassium did not change at all. We conclude that potassium chloride supplements are not an effective treatment of hypokalaemia in this condition. Correction of the extracellular pH by ammonium chloride in 6 patients on chlorthalidone, who demonstrated a slight metabolic alkalosis, gave rise to a mean increase in plasma potassium from 2.78 mEq/l to 2.96 mEq/l (not significant). The hypokalaemia in hypertensive patients on long-term chlorthalidone treatment cannot be explained by either a potassium deficiency or the change in extracellular pH.

Adult↗
PubMed1984

Serum and muscle potassium in experimental alcoholic myopathy.

We investigated the possible role of potassium deficiency, a recognized cause of myopathy, in the pathogenesis of experimental acute alcoholic myopathy (EAM) in the rat. Alcohol-treated animals receiving the same dietary potassium as controls developed mild hypokalemia; however, muscle potassium was preserved or elevated even in the presence of scattered muscle fiber necrosis. Increasing dietary potassium raised serum potassium but did not prevent EAM. These data indicate that hypokalemia in EAM is due to potassium redistribution between intra- and extracellular compartments rather than potassium deficiency, and confirm clinical observations that alcohol-induced muscle injury occurs independently of potassium deficiency.

Acute Disease↗
PubMed2003

Intraerythrocytic potassium levels and early insulin release in children with moderate malnutrition.

Potassium deficiency and insulin releasing defect in severe protein-energy malnutrition (PEM) have been reported previously. The aim of this study was to investigate the existence of potassium deficiency and early insulin releasing defect in moderate PEM, which is more common in children. This study was carried out prospectively in the Pediatrics Department at Trakya University. The study group comprised 30 children with moderate PEM who were also classified as stunted, wasted, and stunting-wasting. Thirty healthy children were selected as controls. Although there was no statistical difference between the study and control groups in terms of serum potassium and initial insulin levels, intraerythrocytic potassium and early insulin release in patients were significantly lower than in controls. The stunting-wasting cases had the lowest intraerythrocytic potassium and early insulin response to intravenous glucose administration. This study suggests that it is appropriate to evaluate moderate PEM cases for intraerythrocytic potassium deficiency and early insulin releasing defect. Potassium supplements should be given if necessary.

Case-Control Studies↗
PubMed1994

Sodium pump current measured in cardiac ventricular myocytes isolated from control and potassium depleted rabbits.

OBJECTIVE: The aim was to investigate cardiac muscle sodium pump function following chronic potassium depletion in rabbits. METHODS: Sodium pump current was measured using the whole cell voltage clamp technique in ventricular myocytes from control rabbits or rabbits with chronic dietary potassium depletion, under conditions designed to minimise all other electrogenic channels, pumps, and exchangers. The effects of changes in external [K+] and intracellular [Na+] were investigated. Experiments were performed on ventricular myocytes enzymatically isolated from adult rabbits, average weight 2.5 kg, which were fed either a control (n = 6), or a potassium deficient diet (n = 8) for 25 d. RESULTS: Potassium depletion significantly increased the sodium pump current density recorded with 10 mM extracellular [K+] and 50 mM [Na+] in the pipette (conditions which activate an estimated 98% of the maximally available pump current), from 1.53(SEM 0.05) pA.pF-1 (control, n = 4) to 1.740(0.06) pA.pF-1 (potassium depleted, n = 4; p < 0.05). The relationship between sodium pump current and extracellular [K+] (30 mM [Na+] in pipette) showed a significant leftward shift in myocytes from potassium depleted animals, such that the Km was reduced from 1.270(0.10) (control, n = 4) to 0.72(0.11) mM (potassium depleted, n = 4; p < 0.05). The effect of varying pipette [Na+] on sodium pump current was examined in cells superfused with 5 mM [K+]. The Km was again reduced from 19.44 mM (control) to 16.91 mM (potassium depleted). The Hill coefficients for activation of the pump by potassium and sodium were essentially unchanged, as was the shape of the current-voltage relationship. CONCLUSIONS: These results suggest that chronic potassium depletion results in an adaptation of the cardiac sodium pump such that pump activity can be maintained, or even enhanced, despite a fall in plasma [K+]. This adaptation is achieved by both alterations in ionic sensitivity to potassium and sodium, and an increase in maximum activity. The latter may reflect an increase in sodium pump site density. These changes are likely to account for the preservation of intracellular [K+] in cardiac muscle during chronic potassium deficiency.

Animals↗
PubMed1993

Potassium regulates plasma testosterone and renal ornithine decarboxylase in mice.

Potassium deficiency produced different effects in the kidney of male or female mice. While in female, potassium deficiency caused a marked renal hypertrophy with no significant changes in testosterone-regulated enzymes, such as ornithine decarboxylase and beta-glucuronidase, in the male the same treatment provoked a marked fall of these enzymes owing to a dramatic decrease in plasma testosterone. Potassium replenishment restored plasma testosterone and renal enzymatic activities. These results show for the first time, that potassium modulates circulating testosterone and suggest that this cation could exert an important regulatory role in controlling androgen actions.

Animals↗