[Potassium chloride poisoning during diabetic coma; significance of the surface potassium gradient on the origin of ECG modifications by action of potassium chloride].
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Diabetes Mellitus↗
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[Study of chronic potassium deficiency in man. I. Influence of rapid changes in blood potassium on urinary potassium output].
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Adult↗
[Diuretics--loss of potassium--potassium deficiency and potassium substitution].
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Diet↗
Hemodynamic, renal, and hormonal responses to changes in dietary potassium in normotensive and hypertensive man: long-term antihypertensive effect of potassium supplementation in essential hypertension.
The hemodynamic, hormonal, and renal responses to alterations in dietary potassium were studied in normotensive and hypertensive subjects. In a short-term study, nine normotensive and nine hypertensive young men received a normal diet and low potassium, high potassium, and high potassium/low sodium diets for 1 week, each. The long-term effect of potassium supplementation (normal diet plus 96 mmol KC1/d for 8 weeks) was evaluated in 17 patients with essential hypertension. Blood pressure did not change significantly during short-term alterations of potassium intake but decreased during long-term supplementation (from 152.2 +/- 3.5/99.6 +/- 1.9 mm Hg to 137.4 +/- 2.9/89.1 +/- 1.4 mm Hg). High dietary potassium induced a significant but transient natriuresis. Plasma potassium concentration was increased during long- but not during short-term high potassium intake. In contrast to plasma renin activity (PRA) and aldosterone, urinary kallikrein was consistently stimulated during long-term potassium supplementation. The plasma concentrations of adrenaline and noradrenaline were significantly higher in hypertensive than in normotensive subjects and were not markedly altered by the dietary changes. It is concluded that long- but not short-term potassium supplementation lowers blood pressure in patients with essential hypertension. The antihypertensive effect may be mediated by potassium-induced natriuresis, by a stimulation of Na-K-ATPase secondary to increased plasma potassium levels, and/or by a modulation of the renin-angiotensin-aldosterone, kallikrein-kinin, and sympathetic nervous systems.
Adult↗
Use of potassium citrate as potassium supplement during thiazide therapy of calcium nephrolithiasis.
The effectiveness of potassium citrate as a potassium supplement was compared to that of potassium chloride in 13 patients with calcium nephrolithiasis treated with thiazide. Thiazide treatment alone reduced serum potassium, urinary calcium and citrate without affecting urinary pH. Urinary saturation of calcium oxalate and brushite decreased but not as much as the decrement in urinary calcium because of reduced citrate-calcium complexation. Potassium chloride supplementation averted thiazide-induced hypokalemia and hypocitraturia without influencing hypocalciuric action of thiazide or urinary pH. The decline in urinary saturation of calcium salts paralleled the decrement in urinary calcium. Potassium citrate supplementation also kept urinary calcium low and corrected hypokalemia. Moreover, it increased urinary pH and citrate above levels in other phases. Thus, the ability of thiazide to lower the urinary saturation of calcium oxalate was accentuated by potassium citrate supplementation but not by potassium chloride supplementation, probably owing to increased citrate complexation of calcium. Moreover, the potassium citrate therapy was more effective than potassium chloride supplementation in reducing the propensity for the spontaneous precipitation of calcium oxalate in urine. In conclusion, potassium citrate supplementation may be superior to potassium chloride supplementation in patients receiving thiazide in whom stones form.
Adult↗
Effect of potassium concentration in dialysate on total body potassium.
OBJECTIVE: To investigate the effects of the presence/absence of potassium in the dialysate on total body potassium content in stable hemodialysis patients. DESIGN: Randomized selection. SETTING: Outpatient chronic hemodialysis unit at the James A. Haley VA Hospital in Tampa, Florida. PATIENTS: Six adult hemodialysis patients (mean age 48 +/- 11.61 years, range 32-65 years) participated in this study. They were all males, four African-Americans and two Caucasians. INTERVENTION: Subjects in a random order received dialysis using a dialysate containing no potassium for 3 months, followed by a 2 mEq/L of potassium for another 3 months. Total body potassium measurements and routine blood analysis were taken at baseline and after each three month period. All subjects received diet instruction pre and monthly on a 3 g/day potassium dietary restriction. MAIN OUTCOME MEASURED: There were no significant differences in the amount of total body potassium concentration between the two different dialysates containing 0 or 2 mEq/L potassium. Mean values of serum albumin were significantly higher when the subjects were dialyzed on a 0 potassium bath. CONCLUSION: The use of dialysate containing 0 or 2 mEq/L potassium concentration does not make a significant difference with regard to total body potassium concentration and maybe advantageous for the patients in terms of more freedom in nutritional intake as demonstrated by a significant increase in serum albumin when they were dialyzed on a 0 potassium bath.
Adult↗
Relation between potassium excretion and proximal tubular fluid output in conscious unoperated rats adapted to different dietary potassium contents.
The effect of dietary potassium content on the proximal tubular fluid output (Vprox), and the relation between Vprox and potassium excretion was examined in conscious unoperated diabetes insipidus rats adapted to five dietary potassium contents in the range 25-400 mmol/kg. The lithium clearance (CLi) and the urine flow (V) were used as measures of Vprox, CLi being equal to and V being about one-third of Vprox. Increase of the dietary potassium content from 25 to 400 mmol/kg led only to a slight, barely statistically significant increase of Vprox. However, repeated measurements in the same rats on different days showed considerable intraindividual variation of Vprox and the potassium excretion. At each dietary potassium level except the lowest one the potassium excretion was linearly correlated to CLi (r = 0.60-0.92) and to V (r = 0.56-0.85). Errors in bladder emptying could not explain these correlations. The slopes of the regression lines increased with increasing dietary potassium content, and the regression lines all intercepted the CLi axis at approximately the same CLi value, i.e., on the average about 70 microliter/min./100 g body weight. The results indicate that an increase of the dietary potassium content leads to a slight increase of Vprox. Spontaneous intraindividual variation of Vprox is considerable and is associated with linearly related variation of the potassium excretion. The change of the potassium excretion for a given change of Vprox increases with the dietary potassium content.
Animals↗
Kaliuresis in normal subjects following oral potassium citrate intake without increased plasma potassium concentration.
Ingestion of potassium salts typically induces both a kaliuresis and an increase in the systemic plasma potassium concentration. In this study normal healthy adults undergoing water diuresis ingested potassium citrate or sodium citrate (0.5 mmol/kg body weight) or continued without ion ingestion (a time control group). Urine was collected over 20-min intervals and venous blood sampled at midinterval. Intake of potassium citrate led to a significant increase in potassium excretion that began during the first postingestion collection and peaked 60-80 min after intake with a maximal increase in potassium excretion above baseline of 1.60 mumol/min.kg-1. The kaliuresis occurred without changes in plasma potassium concentration, excretion of creatinine or calcium, or urine hypo-osmolality and was associated with a briefer, smaller, and less regular increase in sodium excretion and a pronounced but irregular increase in chloride excretion. Plasma aldosterone was insignificantly elevated above baseline, and the initial increase did not occur until 40-60 min after potassium intake. Intake of sodium citrate did not produce a kaliuresis. The cause of the kaliuresis does not appear to be an increased systemic plasma potassium concentration, an increased plasma level of aldosterone, intake of citrate, or an elevated excretion of sodium. The mechanism inducing the kaliuresis following oral potassium intake in the absence of changes in systemic plasma potassium may involve a reflex initiated at potassium sensors in gut, portal vein, or liver.
Administration, Oral↗
Effect of potassium supplementation on blood pressure in African Americans on a low-potassium diet. A randomized, double-blind, placebo-controlled trial.
OBJECTIVE: To determine the effect of potassium supplementation on blood pressure in African Americans consuming a low-potassium diet. DESIGN: Randomized, double-blind, placebo-controlled trial with two parallel arms. SETTING: Community-based research site. PARTICIPANTS: Eighty-seven healthy African Americans aged 27 to 65 years with a systolic blood pressure between 100 and 159 mm Hg and a diastolic blood pressure between 70 and 94 mm Hg. INTERVENTION: During the 21-day intervention period, all participants were provided with a low-potassium diet (32 to 35 mmol/d). In addition to this diet, they were randomly assigned to receive either potassium supplements (80 mmol/d) or placebo. MAIN OUTCOME MEASURE: Change in blood pressure in the potassium vs the placebo group, based on a total of nine blood pressure readings at three visits. Blood pressures were taken before and during the intervention by means of random-zero sphygmomanometry. RESULTS: At baseline, the placebo and potassium groups were similar for mean blood pressure (127/78 vs 125/77 mm Hg), 24-hour urinary potassium excretion (50 vs 44 mmol), and all other variables measured (all P > .05). During the intervention, the net difference in 24-hour urinary potassium excretion between groups was 70 mmol. Compared with the placebo group, the potassium supplementation group experienced a net decline in systolic blood pressure of 6.9 mm Hg (95% confidence interval, -9.3 to -4.4 mm Hg; P < .001) and a decline in diastolic blood pressure of 2.5 mm Hg (95% confidence interval, -4.3 to -0.8 mm Hg; P = .004). Simultaneous adjustment for differences in baseline characteristics only strengthened these estimates. CONCLUSIONS: Potassium supplementation reduces blood pressure substantially in African Americans consuming a diet low in potassium. Increased potassium intake may play an important role in reducing blood pressure in this population at high risk for hypertension.
Adult↗
Stimulatory (insulin-mimetic) and inhibitory (ouabain-like) action of vanadate on potassium uptake and cellular sodium and potassium in heart cells in culture.
(1) The influence of vanadate (Na3VO4) on sodium and potassium uptake as well as on cellular ion contents of sodium and potassium has been studied in heart muscle and non-muscle cells obtained from various species. An ouabain-like inhibition of potassium uptake (up to 50%), combined with a decrease of cellular potassium (up to 20%) has been observed by vanadate (10(-4)-10(-3) M) in heart non-muscle cells obtained from neonatal guinea pigs and chick embryos. In heart muscle and non-muscle cells prepared from neonatal rats, as well as in Girardi human heart cells, a vanadate-induced stimulation of potassium uptake (up to 100%), combined with a rise in cellular potassium (up to 20%) and without significant alteration of cellular sodium, has been found. A slight increase of 22Na+ influx can be measured in rat heart muscle cells and in Girardi human heart cells in the presence of vanadate (10(-4)--10(-3) M). (2) In beating rat heart muscle cells in culture, detrimental effects of serum deprivation--concerning beating properties, potassium uptake and cellular potassium--can at least in part be overcome by addition of vanadate. Furthermore, this compound prevents ouabain-induced signs of toxicity (contractures) in these cells. (3) The stimulatory effects of vanadate on potassium can be mimicked by insulin (1-10 mU/ml). Furthermore, vanadate produces an insulin-like stimulation of 2-deoxy-D-glucose uptake in rat heart muscle and non-muscle cells as well as in Girardi human heart cells. (4) The experimental data demonstrate an ouabain-like inhibition as well as an insulin-mimetic stimulation of potassium-uptake in various heart cells. The reason for this antagonistic mode of action may be due to the different capabilities of the heart cell types to reduce vanadium in the V-valence state of vanadium in the IV-valence state, thereby favouring either ouabain-like inhibition (vanadium V) or insulin-mimetic stimulation (vanadium IV) of potassium transport.
Animals↗
Potassium-magnesium citrate versus potassium chloride in thiazide-induced hypokalemia.
BACKGROUND: The purpose of this study was to compare the value of potassium-magnesium citrate (KMgCit) with potassium chloride in overcoming thiazide-induced hypokalemia. METHODS: Sixty normal subjects first took hydrochlorothiazide (HCTZ; 50 mg/day). After three weeks of treatment (or earlier if hypokalemia developed), they were randomized to take KMgCit (42 mEq K, 21 mEq Mg, and 63 mEq citrate/day) or potassium chloride (42 mEq/day) for three weeks while continuing on HCTZ. RESULTS: KMgCit significantly increased the serum potassium concentration from 3.42 +/- 0.30 mEq/L on HCTZ alone to about 3.8 mEq/L (P < 0.001). Potassium chloride produced a similar increase in serum potassium concentration from 3.45 +/- 0.44 mEq/L to about 3.8 mEq/L (P < 0. 001). KMgCit significantly increased the serum magnesium concentration by 0.11 to 0.12 mEq/L (P < 0.01), whereas potassium chloride produced a marginal decline or no significant change. KMgCit was less effective than potassium chloride in correcting HCTZ-induced hypochloridemia and hyperbicarbonatemia. KMgCit, but not potassium chloride, significantly increased urinary pH (by about 0.6 unit), citrate (by about 260 mg/day), and urinary magnesium. CONCLUSIONS: KMgCit is equally effective as potassium chloride in correcting thiazide-induced hypokalemia. In addition, KMgCit, but not potassium chloride, produces a small but significant increase in serum magnesium concentration by delivering a magnesium load, and it confers alkalinizing and citraturic actions.
Adult↗
[The effect of potassium chloride and organic potassium salts on the acid-base equilibrium in normo and hypokalemic rats].
The effects of intravenous infusions of potassium chloride, potassium acetate, potassium aspartate and potassium malate on plasma electrolytes and acid-base balance were investigated in normokalemic or hypokalemic alkalotic rats. Animals who obtained equal volumes of isotonic sodium chloride solution served as controls. All of these potassium solutions increased the plasma potassium concentrations to the same extent. Potassium chloride shifted the acid-base balance to acidotic values in normal rats or corrected metabolic alkalosis in hypokalemic rats. The potassium salts of organic acids, however, caused an increase in alkalosis, acetate acting stronger than aspartate and malate. In potassium deficiency combined with metabolic alkalosis the administration of potassium chloride is preferable to the organic potassium salts since it corrects both the electrolyte disturbances at the same time.
Acetates↗
In vitro and in vivo assessment of the bioavailability of potassium from a potassium tartrate tablet.
The bioavailability of potassium from orally administered potassium tartrate was evaluated in 20 normal subjects under metabolic balance conditions. Subjects were given 34 mmol potassium (5 tablets of Cal-K) as a divided dose on each of 2 consecutive days. Urinary excretion of potassium, as determined from 24-h urinary collections on the 3 days preceding dosage totalled 192.6 +/- 50.9 mmol (mean +/- S.D., n = 20). It increased significantly (p less than 0.05) to 258.7 +/- 54.2 mmol for the 2 days of dosage and the following day. The difference of 66.1 mmol representing absorbed potassium was close to the 68 mmol potassium given and indicated a bioavailability of potassium in excess of 97 per cent; after correction for creatinine excretion, potassium recovery rose to 99.9 per cent. The dissolution characteristics of the Cal-K tablets were also determined. After dissolution in simulated gastric juice (pH 1.2), 84.4 +/- 10.6 per cent (mean +/- S.D., 6 experiments) was dissolved; after adjustment to pH 7.3, dissolved potassium increased to 91.3 +/- 8.5 per cent. No precipitation or residue formed as a result of the pH change. Both sets of results indicate that potassium from these potassium tartrate tablets is in a highly bioavailable form.
Adult↗
The effect of raising the concentration of potassium in the blood or intestinal lumen on the transport of potassium in the dog intestine.
The rates of transport of potassium, sodium and water across the intestinal mucosa of Thiry-Vella fistulas of colon and ileum, were studied in dogs in two experimental situations; (1) following intravenous infusion of potassium (15 mEg) over 30 minutes and (2) during variations in the intraluminal concentration of potassium in the range 0.8-16.0 mEg/l. Following intravenous infusion of potassium the rates of potassium secretion into the colon were usually increased; the rates of sodium and water absorption were either unchanged or decreased. The unidirectional rate of movement of potassium into the lumen increased as the concentration difference across the mucosa increased; the movement of potassium in the opposite direction remained relatively constant. The undirectional movement of sodium and water into the lumen of the colon also increased but to a lesser extent. The effect on potassium transport in the ileum was not so marked. With increase in the intraluminal concentration of potassium there was a decrease in the rate of net potassium secretion in both colon and ileum. The rates of net absorption of sodium and water were not significantly altered. Unidirectional potassium movement into the body increased in all the ileal fistulas.
Animals↗
Continuous monitoring of potassium efflux from rat parotid gland fragments by potassium selective electrodes.
The concentration of potassium ions in a superfusate of rat parotid gland fragment was continuously monitored by potassium selective electrodes to assess the rate of potassium secretion by the gland. The potassium concentration determined from the electrode readings agreed well with values obtained by atomic absorption (r = 0.99). The detection limit for changes in potassium concentration was approximated to 50 microM K+. When medium was recirculated over the gland fragments it was possible to detect even small changes in the rate of potassium efflux. Thus, increases in potassium secretion following administration of substance P (SP) down to 0.1 nM and carbacholine 10 nM was registered. When the buffer medium was passed only once over the gland fragments it was possible to reproducibly study the time course of potassium secretion. However, with this system higher doses of secretagogues were required for detection of potassium efflux, since the potassium secernated was diluted by the perifused buffer. Following SP (0.01 or 0.1 microM) or carbacholine (1 or 10 microM) a peak of potassium secretion was registered during the first 8-10 min, which was followed by a steady low rate. The metabolic state of the gland fragments, as determined by the ratio of adenine nucleotides, was similar to that found in vivo even after an experiment of several hours' duration. However, the viable part of the glandular tissue, calculated as the content of adenine nucleotides per mg protein, was decreased to approximately 30% compared to the intact gland in situ.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Effect of chronic potassium loading on potassium secretion by the pars recta or descending limb of the juxtamedullary nephron in the rat.
Recently we demonstrated potassium secretion by the pars recta or by the descending limb of the juxtamedullary nephron. The purpose of this present investigation is to study the effect of a chronic high-potassium intake on this phenomenon. Fractional reabsorption of water and sodium by the juxtamedullary proximal nephron was decreased when compared to that in normal hydropenic rats. There was a striking increase in the fraction of filtered potassium at the end of the juxtamedullary descending limb from 94+/11% to 180+/18%, which was principally a result of enhanced potassium secretion. When the concentration of potassium in the collecting tubule fluid of potassium-loaded rats was reduced after the administration of amiloride, a sharp fall was observed in the amount of potassium which reached the end of the descending limb (64+/8%). A direct correlation was observed between the fraction of filtered potassium at the descending limb and the potassium concentration in the final urine (P less than 0.001). The findings suggest that potassium, like urea, normally undergoes medullary recycling, which is enhanced by chronic potassium loading.
Amiloride↗
The effect of dexamethasone on renal potassium excretion and acute potassium tolerance.
In order to further characterize the kaliuretic action of dexamethasone, the effect of the hormone on renal electrolyte excretion and potassium tolerance was evaluated. In the first set of experiments, dexamethasone was administered acutely to unreplaced adrenalectomized rats, to adrenalectomized rats replaced with a single daily injection of dexamethasone (10 micrograms/100 g X day), and to intact control rats. After dexamethasone injection (10 micrograms/100 g), urinary potassium excretion increased by 105% in unreplaced adrenalectomized rats (0.99 +/- 0.13 to 2.02 +/- 0.26 mueq/min, P less than 0.005) and by 59% in rats maintained on glucocorticoid (0.87 +/- 0.10 to 1.38 +/- 0.18 mueq/min, P less than 0.05). The kaliuresis in adrenalectomized rats was associated with a significant increase in phosphate excretion and by a tendency for urinary chloride excretion to rise. In contrast, potassium excretion was unchanged by dexamethasone in control rats. These results indicate that the kaliuretic effect of dexamethasone is influenced by the degree of glucocorticoid deficiency before hormone administration. An additional study with K loading was performed in these same three groups of rats to evaluate the effect of dexamethasone replacement on potassium tolerance. Adrenalectomized rats maintained in daily dexamethasone replacement received an additional dose of hormone (50 micrograms/100 g) before study. After KCl, plasma potassium concentration rose significantly higher in unreplaced adrenalectomized rats vs. control (2.2 +/- 0.2 vs. 1.3 +/- 0.4 meq/liter, P less than 0.05) and peak renal potassium clearance was significantly blunted (577 +/- 90 vs. 1104 +/- 120 microliter/min. P less than 0.001). This impairment in potassium tolerance could not be attributed to hypotension, acidemia, diminished urinary flow, or sodium delivery in the distal nephron in unreplaced adrenalectomized rats but may be explained by decreased renal perfusion since glomerular filtration rate at the end of study was lower than in controls. Dexamethasone replacement improved potassium tolerance (peak delta Pk = 1.7 +/- 0.1 meq/liter) and renal potassium clearance (942 +/- 60 microliter/min). These data demonstrate that dexamethasone, at the high dose employed during KCl loading, improves renal potassium tolerance by enhancing renal K clearance in adrenalectomized rats. These results explain our previous report of near normal potassium excretion in glucocorticoid replaced adrenalectomized rats.
Adrenalectomy↗
Potassium carbonate as a potassium source and dietary buffer for lactating Holstein cows during hot weather.
Twenty-four lactating Holstein cows were offered diets containing .93, 1.29, and 1.53% potassium during hot weather. Cows fed 1.53% potassium consumed more dry matter than cows fed either .93 or 1.29% potassium. Milk production and composition were not different. Potassium intake and fractional excretion increased, and fecal output as a percentage of intake declined with diets containing 1.29 and 1.53% potassium. Magnesium fractional excretion was least and fecal output greatest in cows fed 1.29% potassium. Fecal sodium output and fecal output as a percentage of intake was reduced by 1.53% dietary potassium. During comparison period 2, potassium carbonate at 0, .5, or 1.0% had no effect on feed consumption or milk yield, but buffered diets increased milk fat percentage and depressed milk protein percentage. No effects of buffers on ruminal pH, volatile fatty acids, or digestibility of dry matter or fiber were noted. Cows responded favorably during hot weather to potassium supplementation at 1.53% of the diet, but with high dietary potassium, effects on other minerals must be considered. Chloride, although present above requirements in all diets, was greater in the highest potassium diet.
Animal Feed↗