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PubMed1997

Gossypol-induced hypokalemia and role of exogenous potassium salt supplementation when used as an antispermatogenic agent in male langur monkey.

In our earlier study, we have observed that hypokalemia in langur monkeys, following gossypol acetic acid (GAA) treatment (5 mg dose level) when used as an antispermatogenic agent, and potassium salt supplementation partially maintained body potassium level of the animals. The aims of the present investigation was to confirm further occurrence of hypokalemia in the monkey (comparatively at two higher dose levels) and the role of potassium salt in preventing occurrence of gossypol-induced hypokalemia. Highly purified gossypol acetic acid alone at two dose levels (7.5 and 10 mg/animal/day; oral) and in combination with potassium chloride (0.50 and 0.75 mg/animal/ day; oral) was given for 180 days. Treatment with gossypol alone as well as with the supplementation of potassium salt resulted in severe oligospermia and azoospermia. Animals receiving gossypol alone showed significant potassium deficiency with signs of fatigue at both dose levels. Enhanced potassium loss through urine was found in potassium-deficient animals, whereas animals receiving gossypol acetic acid plus potassium salt showed normal serum potassium with a less significant increase in urine potassium level during treatment phases. Other parameters of the body remained within normal range except gradual and significant elevation in serum transaminases activity. The animals gradually returned to normalcy following 150 and 180 days of termination of the treatment.

Animals↗
PubMed1994

Dietary subacute zinc deficiency and potassium metabolism.

In a controlled animal experiment the effects of dietary subacute Zn deficiency on growth, Zn concentration, and tissue 42-K distribution were studied. Growth retardation caused lower body weight because both skeletal and heart muscle showed a reduction in cell mass. Zn concentrations were reduced in most tissues, however, they remained unaltered in heart muscle. 42-K activity increased in skeletal muscle and pancreas. We hypothesize the latter reflects the organs rate of metabolism, inducing the exocrine pancreas to increase Zn absorption; in skeletal muscle it may induce also alterations in cell potentiation, causing restless behavior. As suggested by the calculated specific K activity (Bq/mol), the K uptake was highest in liver and bone, high in pancreas and skeletal muscle and low in heart muscle. The latter suggests K retention in heart muscle. Specific activity in plasma and jejunum remained unaltered: K status and absorption seem unaffected. Zn deficiency causes different 42-K activities in the various tissues, that respond by alterations in K metabolism without the induction of K deficiency.

Animals↗
PubMed1977

Increased resistance of cystic fibrosis fibroblasts to ouabain toxicity.

Diploid skin fibroblasts derived from several unrelated patients with cystic fibrosis (CF) were tested for resistance to the cytotoxic effects of ouabain in comparison with cells from normal individuals. Cells from CF and normal individuals were plated at low density and exposed to ouabain at different concentrations for 24 hr. Dose-response curves showed that CF cells survived significantly better than did normal cells at all ouabain concentrations from 0.1 nM to 1 micronM in potassium-deficient medium. In medium containing the usual amount of potassium (6.25 mM), survival of the CF cells exposed to ouabain was decreased to that of the normal cells. If the glucose concentration of the potassium-deficient medium was decreased to 10% of the usual amount, the resistance of the CF cells to ouabain disappeared and their survival was identical to that of the normal cells. These findings may be useful in understanding the biochemical basis of CG and its clinical manifestations.

Adolescent↗
PubMed1994

Regulation of rat renal alpha 2 B-adrenergic receptors by potassium depletion.

Potassium depletion and alpha 2-adrenergic receptor (alpha 2-AR) agonists produce similar physiological effects on renal function. Both stimuli increase Na-H exchange in proximal tubule cells, inhibit water transport in collecting tubule cells, and alter blood pressure regulation. The purpose of this study was to determine whether potassium depletion and renal alpha 2-AR subtype expression were linked. Kidney membrane proteins and RNA were harvested from anesthetized rats fed a potassium-deficient diet for 4-20 days (LK 4 to LK 20). Using a selective alpha 2-AR antagonist, [3H]MK-912, we observed that potassium depletion led to a dramatic increase in maximum binding (270% of control) without a change in dissociation constant. Competitive binding studies in LK 14 kidney membranes employing chlorpromazine, prazosin, and oxymetazoline suggested that the increase in alpha 2-ARs in response to potassium depletion was due primarily to an increase in the B subtype of alpha 2-AR. Northern blot analysis demonstrated that renal alpha 2B-AR mRNA levels increased (190% of control) after 4 or 14 days on a potassium-deficient diet. In contrast, there was no difference in steady-state alpha 2A-receptor protein levels by Western blot analysis. We conclude that potassium depletion selectively increases the expression of the B subtype of alpha 2-AR with no detectable effect on alpha 2A-AR expression.

Adrenergic alpha-Antagonists↗
PubMed1961

The renal lesions of electrolyte imbalance. III. The effect of acute chloride depletion and alkalosis on the renal cortex.

Acute chloride depletion in rats is associated with the occurrence of an extensive cell damage in the mid-portion of the proximal convolutions which is followed by an excessive hyperplastic reaction of the renal epithelium; no other significant lesions were found by microdissection in either the tubules of the nephrons or the collecting system. Potassium deficiency is not essential to the development of this lesion but does increase the severity of the reaction. As in the case of potassium deficiency, chloride depletion predisposes to or exaggerates the structural alterations that accompany excess phosphate intake. The relations of the different structural changes in renal architecture that occur in various states of electrolyte imbalance are discussed as well as the relation of the lesions seen experimentally in the rat and monkey and clinically in man.

Alkalosis↗
PubMed1996

A compartmental model predicts that dietary potassium affects lithium dynamics in rats.

Lithium is the treatment of choice for manic depression, but therapy often results in nephrogenic diabetes insipidus and lithium intoxication. To investigate the effects of dietary potassium on potential side effects of lithium therapy, a mathematical model was built using the modeling program SAAM (Simulation, Analysis, And Modeling). Experimental data modeled were from adult male Sprague-Dawley rats fed diets with or without lithium and one of three levels of potassium for 17 d. A five-compartment model of lithium dynamics was built that was consistent with data from rats fed a lithium-containing diet adequate in potassium. This model was then compared with data from rats fed the other two lithium-containing diets. The model predicts that both the fractional transfer coefficient and rate of transport of lithium to the serum compartment from the kidney compartment are lower in rats fed the potassium-adequate diet than in those fed the potassium-deficient diet, and even lower in those fed the potassium-supplemented diet. In addition, fractional transfer coefficients into the serum compartment from the sampled and simulated tissue compartments changed differently with time depending on the amount of dietary potassium. The model also predicts that there would be less accumulation of lithium in the kidney, sampled tissue and simulated tissue compartments with supplemental dietary potassium. The model suggests that potassium supplementation, after a 7-d delay, protects against nephrogenic diabetes insipidus and the potentially toxic accumulation of lithium by decreasing the reabsorption of lithium from the kidneys and increasing lithium efflux from the tissues.

Absorption↗
PubMed2006

Effect of sudden salinity change on Penaeus latisulcatus Kishinouye osmoregulation, ionoregulation and condition in inland saline water and potassium-fortified inland saline water.

Two trials were conducted to determine the effect of sudden decrease in salinity of raw and potassium-fortified inland saline water on western king prawn Penaeus latisulcatus osmoregulation, ionoregulation and condition. Prawns were subjected to salinity decrease over 1 h from 32 to 25 ppt in the first trial and from 27 to 20 ppt in the second trial in three water types: inland saline water with potassium fortified to 100% and 80% of the marine water concentration (IS100, IS80), and raw inland saline water (ISW). In the first trial condition and ingestion rate were monitored over 19 days following salinity change. In the second trial condition, haemolymph osmo- and iono-regulation were recorded over 48 h following salinity change. In the first trial, 100% mortality was observed in ISW by day 13, with final survival 94% in IS80 and 100% in IS100. Tail muscle moisture content increased significantly (P < 0.05) over time in both trials and in all water types, suggesting loss of energy reserves. In the second trial, serum osmolality, sodium concentration and osmoregulatory capacity decreased following salinity change, stabilising by 24 h in IS100 and IS80 but continuing to decrease till 48 h in ISW, suggesting partial breakdown of osmoregulatory function in the potassium-deficient medium. Prawns were stronger regulators of divalent than monovalent cations. These trials demonstrate that potassium-deficient inland saline water requires fortification with potassium to allow prawn survival and efficient osmoregulation.

Animals↗
PubMed1992

Sudden unexplained death syndrome. A review and update.

Sudden unexplained death syndrome (SUDS) among young healthy Thai construction workers in Singapore has been given much publicity recently. From May 1982 to July 1990, 226 SUDS were reported among them. In this article we review and compare studies on SUDS in the United States and South-east Asia. So far, studies to identify the causal factors have been inconclusive and they cannot explain the male preponderance and occurrence of death during sleep. Current hypotheses about the cause of SUDS have included stress, genetic factors, dietary deficiency (particularly thiamine), potassium deficiency, melioidosis and sleep disorders. The following areas are suggested for further research: epidemiological investigations on SUDS at its source; in-depth case studies of families with and without SUDS; role of dietary factors, biochemical studies with respect to thiamine, pyruvate and potassium metabolism in the victims and susceptibles; and histopathological studies of cases and controls.

Adolescent↗
PubMed1987

Effect of potassium depletion and protein intake in vivo on renal tubular bicarbonate transport in vitro.

These studies evaluated the effect of decreased dietary potassium and increased dietary protein content in rabbits on systemic acid-base parameters, urine pH, and segmental renal tubular bicarbonate handling in vitro. Animals fed a potassium-deficient high-protein diet (KD) for 2 wk developed metabolic acidosis (arterial blood pH 7.31 vs. 7.43) and excreted a more acid urine than control animals fed a diet with normal amounts of potassium and protein; whereas, animals fed the same potassium deficient diet to which supplemental potassium was added (KD + K+) excreted an even more acid urine and had a blood pH of 7.36. In superficial proximal convoluted and straight tubules, there were no differences in rates of fluid and total CO2 absorption between control and KD tubules. Cortical collecting tubules obtained from KD and KD + K+ animals absorbed, and control tubules secreted total CO2 in vitro. With an ambient potassium concentration of 2.5 mM, collecting tubules obtained from the inner stripe of the outer medulla of KD animals absorbed significantly less total CO2 than control tubules. The same tendency was observed in collecting tubules from the outer stripe of the outer medulla. Plasma aldosterone levels fell with development of potassium depletion. Administration of deoxycorticosterone for 1 day to KD animals was associated with a lower urine pH and higher arterial blood pH than in untreated KD animals and with increased total CO2 absorption by both cortical collecting tubules and tubules from the inner stripe of the outer medulla.(ABSTRACT TRUNCATED AT 250 WORDS)

Absorption↗
PubMed1980

Basic amino acid accumulation in potassium-depleted rat muscle.

In rat muscle, a depletion of potassium is partially compensated for by a gain of sodium. In addition cationic (free basic) amino acids accumulate in the muscle of the potassium-deficient rat. A 31% muscle potassium depletion was induced by dietary restriction of potassium in two groups of rats which differed in the test diet content of lysine and arginine (adequate and excessive). The excess lysine and arginine accumulation in the muscle of the rats fed excess levels of lysine and arginine was accompanied by an equimolar reduction in the gain of sodium. The results demonstrate that lysine and arginine accumulation consists of a transfer of positive charges in compensation to the charges lost with potassium, and that cationic amino acids may spare the role of sodium under these conditions.

Amino Acids↗
PubMed1981

Impairment of testicular maturation in potassium depleted pre-pubertal rats.

When maintained on a potassium deficient diet 21 day-old weanling rats ceased to grow. At the end of 3 weeks, the testes were small and the diameter of seminiferous tubules was reduced. The reduction of the tubular diameter resulted mainly from a decrease in the number of cells, chiefly spermatids. An occasional tubule contained a few scattered spermatozoa. Ultrastructurally, the cytoplasm of Sertoli cells contained an increased number of lipid droplets as well as phagocytosed degenerative cells. Spermatids, conspicuously fewer in number, showed abnormal forms and did not mature beyond the early acrosomic phase. It appeared then, that potassium deficiency in immature rats not only arrested growth but largely prevented spermatogenesis. This probably resulted from a widespread inhibition of pituitary trophin function. Also, the deleterious effects on spermatids could be due to local lack of potassium which is present in high concentration in normal seminiferous tubular lumen.

Animals↗
PubMed1982

Formation of Crystalline delta-Endotoxin or Poly-beta-Hydroxybutyric Acid Granules by Asporogenous Mutants of Bacillus thuringiensis.

Parental strains and asporogenous mutants of Bacillus thuringiensis subspp. kurstaki and aizawai produced high yields of delta-endotoxin on M medium, which contained 330 mug of potassium per ml, but not on ST and ST-a media, each of which contained only 11 mug of potassium per ml. On ST and ST-a media, refractile granules were formed instead. These granules had no insecticidal activity against silkworms and were isolated and identified as poly-beta-hydroxybutyric acid. Supplementation of the potassium-deficient ST-a medium with 0.1% KH(2)PO(4) (3.7 mM) led to the formation of crystalline delta-endotoxin. The replacement of KH(2)PO(4) with equimolar amounts of KCl, KNO(3), and potassium acetate or an equivalent amount of K(2)SO(4) had a similar effect, whereas the addition of an equimolar amount of NaH(2)PO(4) or NH(4)H(2)PO(4) did not cause the endotoxin to form. An asporogenous mutant, B. thuringiensis subsp. kurstaki strain 290-1, produced delta-endotoxin on ST-a medium supplemented with 3 mM or more potassium but formed only poly-beta-hydroxybutyric acid granules on the media containing </=1 mM potassium. These results clearly indicate that a certain concentration of potassium is essential for the fermentative production of delta-endotoxin by these isolates of B. thuringiensis. Manganese could not be substituted for potassium. Phosphate ions stimulated poly-beta-hydroxybutyric acid formation by strain 290-1. The sporulation of B. thuringiensis and several other Bacillus strains was suppressed on the potassium-deficient ST medium. This suggests that potassium plays an essential role not only in Bacillus cell growth and delta-endotoxin formation but also in sporulation.

Journal Article↗
PubMed1972

On the mechanism of rhabdomyolysis in potassium depletion.

Rhabdomyolysis and myoglobinuria occur commonly in men who sustain environmental heat injury during intensive physical training in hot climates. These also occur in patients with potassium depletion. Since physical training in hot climates may be accompanied by serious losses of body potassium, the possibility was considered that performance of strenuous exercise when potassium deficient might enhance susceptibility to rhabdomyolysis. Potassium is released from contracting skeletal muscle fibers and its rising concentration in interstitial fluid is thought to dilate arterioles thereby mediating the normal rise of muscle blood flow during exercise. If potassium release from deficient muscle were subnormal, exercise would not be accompanied by sufficient muscle blood flow and rhabdomyolysis could occur by ischemia. This hypothesis was examined by comparing the effect of electrically stimulated exercise on muscle blood flow, potassium release, and histology of the intact gracilis muscle preparation in normal and potassium-depleted dogs. In normal dogs, muscle blood flow and potassium release rose sharply during exercise. In contrast, muscle blood flow and potassium release were markedly subnormal in depleted dogs despite brisk muscle contractions. Although minor histologic changes were sometimes observed in nonexercised potassium-depleted muscle, frank rhabdomyolysis occurred in each potassium-depleted animal after exercise. These findings support the hypothesis that ischemia may be the mechanism of rhabdomyolysis with exercise in potassium depletion.

Animals↗
PubMed1985

Gossypol-hypokalaemia interrelationships.

Around 1% of 8806 volunteers taking gossypol as a male contraceptive had hypokalaemic paralysis and more had simple hypokalaemia, the direct cause being renal potassium loss. In gossypol takers not showing hypokalaemia, serum potassium levels were within the normal range but were significantly lower than levels in controls. In the majority of patients suffering from gossypol-induced hypokalaemia, recovery was prompt and complete following potassium repletion, but in some men there were recurrent attacks of hypokalaemia during a period of several months to years after cessation of gossypol treatment. The incidence of hypokalaemic paralysis in gossypol takers showed distinct regional differences, being much higher in Nanjing, where the dietary potassium level of the inhabitants was low, than in Taian, where the dietary potassium level was high. In rats fed a low-K fodder, gossypol reduced the intracellular Mg and K concentrations of the skeletal muscle, while in regularly fed rats, this effect of gossypol was not observed. A potassium deficient diet could thus be considered a contributing factor in the development of gossypol-induced hypokalaemia. Potassium deficiency has also been shown to enhance the anti-spermatogenic effect of gossypol. Suggested mechanisms for the development of gossypol-induced hypokalaemia include inhibition of Na-K-ATPase activity, stimulation of prostaglandin biosynthesis, damage to the renal tubule, and modification of membrane transport.

Contraceptive Agents, Male↗
PubMed1990

[2 cases of severe hypokalemia with acute rhabdomyolysis].

We report two cases of acute rhabdomyolysis due to severe hypokalemia. The first case appears to be caused by a chronic dietary potassium deficiency, responsible also for the elevation of blood pressure and the impairment of myocardial contractility. The administration of hydrochlorothiazide, albeit associated with captopril, could have decompensated the potassium balance, thus precipitating the acute rhabdomyolysis. More commonly the second case is due to acute potassium losses induced by a trivial enteritis in a hypertensive patient who was taking thiazide diuretics for a long period of time. We emphasize that chronic dietary potassium deficiency may represent a predisposing variable to acute rhabdomyolysis, which is generally precipitated by the superimposition of other potassium lowering factors.

Acute Disease↗
PubMed1984

Diuretics, potassium depletion and the risk of arrhythmias.

Evidence is available which suggests that the use of thiazide diuretics in the treatment of essential hypertension causes a fall in both plasma and total body potassium. The incidence of ventricular arrhythmias is proportional to the potassium deficit and may be enhanced by concomitant magnesium deficiency. Potassium loss may be minimized by limiting the dose of diuretic and by restricting sodium intake. Potassium chloride supplements are of relatively limited value and potassium-conserving diuretics are to be preferred in aviators. To reduce the potential risk of rhythm disturbance, aircrew receiving thiazide diuretics should be managed to ensure a serum potassium level at least 3.5 mmol l-1 after stabilization on therapy.

Aerospace Medicine↗
PubMed1959

Effect of various electrolytes upon cardiac and skeletal musculature.

In rats kept on a low-potassium diet that contains only maintenance levels of magnesium, cardiac necroses and muscular cramps were readily induced by the oral administration of sodium perchlorate or disodium hydrogen phosphate. The precipitation of these cardiac and skeletal muscle changes by sodium chlorate was prevented by the prophylactic administration of either potassium or magnesium chlorides. The protective effect of these chlorides against the cardiotoxic and convulsive effects of disodium hydrogen phosphate has already been demonstrated by our earlier experiments. Sodium sulphate produced cardiac necroses in rats maintained on the same diet, and both potassium and magnesium chlorides had a prophylactic action. Unlike sodium perchlorate, however, sodium sulphate produced no muscular cramps under these conditions. Equimolecular amounts of sodium given in the form of sodium chloride (instead of sodium perchlorate, sodium sulphate, or disodium hydrogen phosphate) did not cause cardiac necroses or muscular cramps in rats maintained on the potassium-deficient diet. As the same three sodium salts, namely the perchlorate, the sulphate, and the hydrogen phosphate, produced cardiac necroses in rats sensitized by either a potassium-deficient diet or by certain corticoids, it seems that the anion must play a decisive rôle, since equivalent amounts of NaCl are ineffective.

Animals↗