Total body potassium in protein calorie malnutrition.
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Child, Preschool↗
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[The potassium content of mushrooms (author's transl)].
The potassium content of 410 species (1075 samples) of wild mushrooms ranged between 1.5 and 117g/kg dry wt. It was dependent on species and genus, and on the average was highest in Coprinaceae and lowest in Polyporaceae. A positive correlation was observed between potassium and water content; consequently, the potassium content of the wet wt. showed less variation: it ranged between 0.6 and 14.6 g/kg. In the solid matter of single fruit-bodies (11 species) potassium was distributed as follows: flesh of the cap greater than stem greater than gills or tubes greater than spores. The flesh of the cap contained maximally 1.8 times the potassium of the gills. But due to a correspondingly higher water content, significant potassium differences between fresh weights of these parts of fruit-bodies were uncommon. Potassium was concentrated 20--40-fold in fruit-bodies as compared with the soil.--According to our results mushrooms rank among the most potassium-rich vegetables, appropriate for consideration in diets in chronic potassium deficiency. On the other hand, toxic effects must be considered, especially in cases of renal insufficiency.
Basidiomycota↗
Evidence for the presence of separate mechanisms regulating potassium and sodium distribution in Ulva lactuca.
1. The methods employed in these and preceding (25-27) studies were shown to allow analysis of true cellular sodium and potassium concentrations. 2. The rate of reaccumulation of potassium by potassium-deficient cells is independent of the presence or absence of sodium in the external medium. 3. Phenylurethane (10(-3)M), a photosynthetic and metabolic inhibitor, causes a marked progressive loss of potassium and gain of sodium, both of which changes are completely reversible on transferring the samples to running sea water. 4. Iodoacetate, while not effective in causing potassium and sodium shifts in the light, effects a loss of potassium and a gain of sodium in the light in the presence of phenylurethane. 5. Arsenate (5 x 10(-3)M) completely protects Ulva against the potassium loss usually observed with iodoacetate in the dark while it affords no protection against the sodium influx under the same conditions. Arsenate given after 18 to 20 hours in iodoacetate gives significant protection against potassium loss in the dark, and allows a slight net reaccumulation of potassium in the light. Arsenate in the dark after iodoacetate affords no protection against the sodium uptake caused by iodoacetate in the dark, while in the light under the same conditions sodium is rapidly secreted to the control level within a few hours. This resecretion of sodium is thought to be primarily an effect of light, the presence of arsenate being incidental. 6. The "decoupling agent" 4,6-dinitro-o-cresol causes a marked progressive increase in cellular sodium and a drop in cellular potassium, though the kinetics of these two movements are distinctly different from each other. 7. Pyruvate (50 mg. per cent) given with iodoacetate (2 x 10(-3)M) for 5 hours in the dark completely prevents the sodium increase caused by iodoacetate, while affording less protection against the potassium loss. Phosphoglycerate, on the other hand, offers more protection against potassium loss, and essentially none against the sodium gain. 8. ATP added in small amounts at short intervals to samples maintained in 10(-3)M iodoacetate in the dark affords significant protection against the potassium loss observed in iodoacetate. Cellular sodium is somewhat higher in the ATP-iodoacetate samples than in the iodoacetate samples. 9. In the discussion of the data presented two major points are emphasized: (1) the close correlation between cellular metabolism and normal cation control; (2) two mechanisms must be operative in cation regulation in this organism: one for moving potassium inwards and the other for transporting sodium outwards. These mechanisms are independent of each other.
Eukaryota↗
Effect of applications of sewage sludge on N, P, K, Ca, Mg and trace element contents of plant tissues.
A four-month study was conducted in a greenhouse with Larix laricina grown on sand and nursery soil. This culture was fertilized with anaerobically digested sludge at various rates and doses. No direct relationship could be established between the growth of seedlings and the quantities of sludge applied. Relationships were, however, established between the quantities of sludge applied and the elemental composition of the tissues. There was a significant, positive correlation between the growth of seedlings and the phosphorus and nitrogen content of their tissues. These elements originated from the wastewater sludge. Tissues had potassium deficiencies and an excess of calcium, magnesium and trace elements.
Calcium↗
Red-blood-cell potassium and hand-grip strength in healthy elderly people.
Red-blood-cell potassium (RBCK) as an indicator of body potassium status was measured in 103 healthy elderly subjects over the age of 65 years. There was no correlation between RBCK and grip strength. The only significant predictors of grip strength were age and sex. The RBCK values formed a single normal distribution. There was no hypokalaemic subpopulation such as would be expected if potassium deficiency were common in these old people.
Age Factors↗
Application of multivariate autoregressive modelling for analysing chloride/potassium/bicarbonate relationship in the body.
The authors repeatedly analysed course data of acid-base disturbances accompanying hypochloraemia and/or hypokalaemia by means of multivariate autoregressive modelling. It was found that the regulatory relationship between chloride and bicarbonate is inverse between the following two hypochloraemic hyperbicarbonataemic states: the one induced by chloride depletion and the other induced by CO2 retention. Also, the study revealed an independent role of potassium deficiency in the development of metabolic alkalosis, especially in cases with mineralocorticoid-induced alkalosis. The present approach enabled the authors to solve a long-standing problem, i.e. to differentiate between the roles of chloride and potassium in the development of metabolic alkalosis.
Alkalosis↗
[Treatment of colectasia occurring in intensive care].
Acute false colonic obstruction occurred in one female and nine male patients aged between 51 and 82 years. They had been admitted to an intensive care unit for respiratory failure (thoracic trauma, pneumonia, chronic or postoperative respiratory failure, or neurological disease). Three patients were in terminal multiple organ failure. There was an associated potassium deficiency in six of the patients. Mechanical ventilatory support was required in eight patients. Plain abdominal X-rays showed caccal diameters greater than 8 cm, confirming the diagnosis. All these patients were initially treated with nasogastric suction, intravenous fluids, potassium replacement, but without success, except in one patient. One spontaneous caecal perforation and a case of impending perforation were treated surgically without prior endoscopy. Nine colonoscopies were carried out with great difficulties. Immediate colic deflation was achieved, but the colic distension resumed 24 h later in six patients. Normal bowel function restarted after colonoscopy in one patient, whilst another one perforated. The air introduced during colonoscopy in the already distended bowel may have speeded up the perforation. Surgery (caecostomy or colostomy) was followed by a return to normal bowel function in seven out of eight patients. One patient died as a result of his spontaneous caecal perforation; the death of three other patients was due to the underlying disease. Ogilvie's syndrome occurring in intensive care patients requires colonic decompression to avoid perforation. Colonoscopy helps to rule out true anatomic occlusion and confirms the diagnosis. However, it is often difficult to carry out, poorly efficient and sometimes dangerous.(ABSTRACT TRUNCATED AT 250 WORDS)
Aged↗
Differing effects of supplemental KCl and KHCO3: pathophysiological and clinical implications.
Compared to the prehistoric diet, the modern human diet contains not only excessive NaCl and deficient K+, but also deficient precursors of HCO3- and sometimes excessive precursors of nonvolatile acid. The mismatch between the modern diet and the still ancient biological machinery of humans subtly but chronically disorders their internal milieu, giving rise to a prolonged state of low-grade potassium deficiency and low-grade metabolic acidosis whose severity increases with age. Supplemental KCI cannot redress this mismatch and correct this state. However, the mismatch is redressed and the state corrected by restoring intakes of K+ and HCO3- to levels approaching those in the diet of our prehistoric forebearers, with either fruits and vegetables or with supplemental KHCO3. So restored, KHCO3 can: 1) attenuate hypertension and possibly prevent its occurrence by suppressing the phenomenon of normotensive NaCl-sensitivity, in part by its natriuretic effect; (2) prevent kidney stones by reducing urinary excretion of calcium and increasing urinary excretion of citrate; (3) ameliorate and protect against the occurrence of osteoporosis by increasing the renal retention of calcium and phosphorus, and by suppressing bone resorption and enhancing bone formation; and (4) likely prevent stroke.
Adult↗
A possible low intracellular potassium in obesity.
In comparison with lean marathon runners whose fat content was 15%, obese subjects with a fat content of 55% showed a 36% reduction in intracellular potassium. It is hypothesized that as much as 60% of this decrease may have been due to the lower proportion of muscle (which has the highest intracellular potassium of any tissue) in the fat free mass of very obese subjects. The remainder of the decrease seems to have been a measurement artefact owing to self-absorption of gamma rays by adipose tissue, most of which is distributed over potassium rich lean tissue. The low intracellular potassium values found in obesity should not be interpreted as necessarily signifying potassium deficiency.
Adipose Tissue↗
Effect of dietary potassium percent for lactating dairy cows.
Three groups of Holstein cows (four cows per group) past the peak of lactation were fed dietary potassium as percent of dry matter as follows: .45% for 20 days to all groups; .45, .55, and .66% to the respective groups for 12 wk; and .66% to all groups for 19 days. Dietary potassium had no significant effect on milk fat and solids-not-fat contents of milk, milk production, or milk and blood serum cations (potassium, sodium, magnesium, calcium). However, body weights were affected. Symptoms common in potassium deficiency were not apparent. Average daily milk production, feed intake, and body weight gains for the 12 wk in kilograms were: 21.9, 15.8, and 15.7; 23.4, 16.4, and 54.5; and 22.8, 19.9, and 92.9 for the .45, .55, and .66% rations. When .66% potassium was fed to groups previously fed .45 and .55% potassium, feed intake increased by 3.6 kg and 1.3 kg but increased only .2 kg in the group previously fed .66%.
Animals↗
Hypokalemic myopathy during treatment with diuretics.
Two male patients with severe reversible muscle weakness and excessive potassium deficiency associated with alkalosis during treatment with diuretics are presented. The case reports are further illustrated by the morphologic changes as seen in light and electron microscopic examination of muscle biopsies. Hypokalemia and muscle dysfunction are discussed in relation to other investigations of altered potassium metabolism and myopathy during treatment with certain diuretics.
Chlorthalidone↗
Potassium depletion modulates aldose reductase mRNA in rat renal inner medulla.
The organic osmolytes present in renal inner medullary cells balance the extracellular hyperosmolality and protect the cell against the effects of high salts and urea. We previously demonstrated that a renal concentrating defect due to potassium depletion was associated with a decrease in organic osmolytes including sorbitol. However, we could not determine whether a reduction in medullary organic osmolyte would be cause or effect of urine concentration defect associated with potassium depletion. We focused on the synthesis of sorbitol catalyzed by the enzyme, aldose reductase. To clarify whether the treatment of potassium depletion would affect aldose reductase when extracellular tonicity, and medullary sodium or potassium was maintained at the level of control rats, we administered a hypertonic solution of NaCl or KCl to potassium-depleted rats and evaluated aldose reductase enzymatic activity and mRNA abundance as well as the medullary contents of organic osmolytes. Either infusion significantly reduced tissue sodium content in potassium-depleted rats. With KCl infusion protocol but not that of NaCl, sorbitol as well as aldose reductase mRNA abundance increased to the control level. Medullary contents of other organic osmolytes exhibited a pattern similar to sorbitol. Data suggested that aldose reductase mRNA abundance was reduced in potassium depletion irrespective of medullary sodium content. A decrease in sorbitol level may precede a urinary concentrating defect. Our finding constitutes the first demonstration of the relationship between a potassium deficiency and the abundance of aldose reductase mRNA, an osmoregulatory protein in the kidney.
Aldehyde Reductase↗
Contrasting effects of various potassium salts on renal citrate excretion.
Mechanisms for the citraturic response to potassium citrate treatment were sought by assessing renal citrate clearance and acid-base status after oral administration of potassium citrate, potassium bicarbonate, and potassium chloride. After 2 weeks of treatment of eight patients with stones at a dose of 80 meq/day, urinary citrate rose significantly from 2.5 +/- 1.6 mmol/day (no drug) to 5.1 +/- 1.7 mmol/day with potassium citrate and to 4.5 +/- 1.5 mmol/day with potassium bicarbonate (P less than 0.05), but did not change significantly with potassium chloride. Citrate clearance increased from 8.0 to 27.4 mL/min with potassium citrate and 25.8 mL/min with potassium bicarbonate (P less than 0.05), but did not increase with potassium chloride. Both potassium citrate and potassium bicarbonate significantly raised urinary bicarbonate and decreased urinary ammonium, titratable acid, and net acid excretion. Potassium chloride was without effect. Effects of potassium citrate on urinary citrate, citrate clearance, and acid-base status tended to be more prominent than those of potassium bicarbonate, but these changes were not significant. Thus, the citraturic action of potassium citrate is largely accountable for by provision of an alkali load. Potassium itself had no effect in the absence of potassium deficiency.
Adult↗
Oral administration of magnesium hydroxide to subjects with insulin-dependent diabetes mellitus: effects on magnesium and potassium levels and on insulin requirements.
Intra- and extracellular levels of magnesium and potassium were determined in 16 subjects with insulin-dependent type I diabetes mellitus (IDDM) and 30 healthy controls. Subjects with IDDM had lower levels of magnesium in muscle biopsies (p less than 0.001), plasma (p less than 0.001), and mononuclear cells (p less than 0.05), and higher urinary excretions of magnesium (p less than 0.01), and lower levels of potassium in muscle biopsies (p less than 0.001), and erythrocytes (p less than 0.05), as compared with those in controls. Magnesium hydroxide (500 mg/day) was administered orally to the diabetics. The levels of magnesium and potassium in muscle biopsies increased (p less than 0.001; p less than 0.001), while the plasma levels of magnesium and the urinary excretions of magnesium increased only temporarily, during 21 weeks of treatment. The requirements of insulin were reduced (p less than 0.001) during the course of the study, whereas the levels of glycosylated hemoglobin (HbA1c) and glucose were not changed. The findings indicate that administration of magnesium hydroxide is useful to treat muscular magnesium and potassium deficiency in diabetics.
Adult↗
Potassium supplementation improves the natriuretic response to central volume expansion in primary aldosteronism.
Potassium depletion induced by dietary potassium restriction is known to cause sodium retention, while potassium supplementation is known to increase urinary sodium excretion. However, the ability of potassium deficiency to affect mineralocorticoid-induced sodium retention in aldosterone-producing adenoma (APA) subjects has not been extensively investigated, neither in baseline conditions nor when facilitating natriuresis through a physiological manoeuver such as central blood volume expansion. With the aim of testing the hypothesis that potassium supplementation would attenuate the mineralocorticoid-induced sodium retention, in 7 APA patients elevation of serum potassium was obtained by infusion of isosmotic potassium chloride (KCl) at a constant rate of 36 mmol/h for a 2-hour period for 5 consecutive days. The same patients were also submitted to acute central volume expansion by head-out water immersion (WI) associated with either low or normal serum potassium levels. The assessment of natriuresis in baseline condition and during WI was also performed in 10 age-matched control subjects. Central hypervolemia by WI induced a significant natriuretic response in APA hypokalemic subjects; on the other hand, in the same APA subjects giving potassium supplementation, WI-induced urinary sodium excretion was significantly higher (P <.001) than that obtained during WI at normal potassium intake (hypokalemic condition). Blood pressure responses and hormonal profiles were almost superimposable during the 2 WI experiments performed at different serum potassium levels. By confirming that amelioration of hypokalemia attenuates mineralocorticoid-induced sodium retention, this study also suggests that potassium intake may represent an important determinant of mineralocorticoid escape.
Adult↗
Electrolyte balance in gastrointestinal disease.
Even small losses of gastrointestinal secretions when combined with reduced intake of electrolytes may seriously disturb electrolyte balance. Knowledge of the ionic composition of secretions lost is essential in planning therapy. Loss of gastric contents usually results in excessive loss of chloride; in achlorhydria this is not the case. Loss of sodium and potassium may be large in either case and is often underestimated. Small bowel obstruction results in a more balanced loss of electrolyte which may not affect acidbase balance greatly. In diarrhea loss of base predominates, and may result in a large potassium deficit. Steatorrhea due to nontropical sprue results in large fecal losses of sodium, potassium and chloride, in addition to the large calcium and phosphorus loss. In chronic peptic ulcer excessive ingestion of milk and absorbable alkalies may result in hypercalcemia, azotemia and alkalosis, without hypercalciuria. Since renal function is usually adequate in the milder gastrointestinal disturbances, electrolyte and fluid replacement should be started early, and can be guided by generally available laboratory tests, the carbon dioxide combining power and serum chloride levels, provided the predominate ionic loss is known and potassium deficiency remedied. If this is done, development of serious fluid and electrolyte deficits can usually be prevented.
Alkalosis↗
[Exchange of putrescine and potassium between cells and media as a factor in the adaptation of Escherichia coli to hyperosmotic shock].
Putrescine/potassium exchange in response to hyperosmotic stress was studied. The addition of 0.3 M NaCl or 0.44 M sucrose to an exponentially growing E. coli culture induced potassium uptake and putrescine release from the cell. Potassium added to an osmotically stressed potassium-deficient culture was readily absorbed by cells; this was accompanied by the loss of intracellular putrescine, both free and bound. Since DNA is the main binding site of putrescine, the loss of bound putrescine caused a relaxation of DNA supercoiling. The increase in the intracellular content of potassium not only restored but also enhanced DNA supercoiling as compared to the initial level. In vitro experiments showed the degree of plasmid DNA supercoiling to rise drastically at potassium concentrations of 300-500 mM, while different putrescine concentrations affected this parameter differently. Thus, the physiological concentrations of putrescine (below 1 mM) greatly augmented DNA supercoiling, whereas higher concentrations (5-10 mM) exerted a relaxing effect. A change in DNA supercoiling in vivo in response to osmotic stress is the result of competition between biogenic and abiogenic cations for the sites of binding to polyanionic DNA structures. A change in DNA topology serves as the regulatory factor controlling the expression of genes responsible for cell adaptation to osmotic stress.
Adaptation, Physiological↗
Hypokalemic rhabdomyolysis associated with Bartter's syndrome.
Severe potassium deficiency is an uncommon cause of rhabdomyolysis. We recently treated a 45-year-old patient with myalgia, serious generalized weakness, increased serum creatine kinase and myoglobin level as well as excessive hypokalemia. Histological examination of deltoid muscle biopsy showed rhabdomyolysis. After complete recovery of muscle damage by potassium substitution Bartter's syndrome proved to be the cause of initial and persistent hypokalemia.
Bartter Syndrome↗