[Diagnosis of potassium depletion in a cardiology ward. Value of the measurement of exchangeable potassium and erythrocyte potassium].
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Diuretics↗
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A comparison of potassium bicarbonate and potassium chloride in the repair of potassium deficiency.
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Acid-Base Equilibrium↗
Potassium loading effect on potassium balance in athletes during prolonged restriction of muscular activity.
Negative potassium balance during hypokinesia (decreased number of kilometers taken/day) is not based on the potassium shortage in the diet, but on the impossibility of the body to retain potassium. To assess this hypothesis, we study the effect of potassium loading on athletes during prolonged hypokinesia (HK). Studies were done during 30 d of a pre-HK period and during 364 d of an HK period. Forty male athletes aged 23-26 yr were chosen as subjects. They were divided equally into four groups: unloaded ambulatory control subjects (UACS), unloaded hypokinetic subjects (UHKS), loaded hypokinetic subjects (LHKS), and loaded ambulatory control subjects (LACS). For the simulation of the hypokinetic effect, the LHKS and UHKS groups were kept under an average running distance of 1.7 km/d. In the LACS and LHKS groups, potassium loading tests were done by administering 95.35 mg KCl per kg body weight. During the pre-HK and HK periods and after KCl loading tests, fecal and urinary potassium excretion, sodium and chloride excretion, plasma potassium, sodium and chloride concentration, and potassium balance were measured. Plasma renin activity (PRA) and plasma aldosterone concentration was also measured. Negative potassium balance increased significantly (p < or = 0.01) in the UHKS and LHKS groups when compared with the UACS and LACS groups. Plasma electrolyte concentration, urinary electrolyte excretion, fecal potassium excretion, PRA, and PA concentration increased significantly (p < or = 0.01) in the LHKS and UHKS groups when compared with LACS and UACS groups. Urinary and fecal potassium excretion increased much more and much faster in the LHKS group than in the UHKS group. By contrast, the corresponding parameters change insignificantly in the UACS and LACS groups when compared with the base line control values. It was concluded that urinary and fecal potassium excretion increased significantly despite the presence of negative potassium balance; thus, negative potassium balance may not be based on potassium shortage in the diet because of the impossibility of the body to retain potassium during HK.
Adult↗
Relationship between plasma potassium concentration and renal potassium excretion.
To study the relationship between extracellular potassium concentration and renal excretion of potassium, seven chronically adrenalectomized dogs were maintained on a constant intravenous infusion of aldosterone (50 micrograms/day), and constant sodium intake (30 meq/day ) while they received four levels of potassium intake--10, 30, 100, and 200 meq/day--for 7-10 days each. At the conclusion of each level of intake, plasma potassium and renal excretion as well as other variables known to influence potassium excretion were measured. There were minimal changes in arterial pH, mean arterial pressure, extracellular fluid volume, or glomerular filtration rate at any level of potassium intake. The values for plasma potassium and renal potassium excretion attained at each level of intake were: 3.13 +/- 0.24 and 10 +/- 2; 4.18 +/- 0.18 and 21 +/- 6; 4.31 +/- 0.11 and 66 +/- 10; and 4.75 +/- 0.10 meq/liter and 170 +/- 16 meq/day, respectively. Under these experimental conditions in which the levels of aldosterone, sodium intake, arterial pH, arterial pressure, extracellular fluid volume, and glomerular filtration rate remain constant, plasma potassium concentration appears to have a week effect on renal potassium excretion below the normal level of plasma potassium (approx. 11 meq/day change in excretion for each milliequivalent per liter change in concentration). Above the normal level, however, plasma potassium concentration has a powerful effect, 260 meq/day per milliequivalent per liter. The characteristics of the relationship between plasma potassium and renal potassium excretion make it ideally suited for controlling potassium excretion in response to greater than normal potassium intake.
Adrenalectomy↗
The influence of potassium administration and of potassium deprivation on plasma renin in normal and hypertensive subjects.
The effect of potassium administration and of dietary potassium deprivation on plasma renin activity and aldosterone excretion has been studied in 10 normal subjects and in 12 hypertensive patients maintained on a constant dietary regimen. Potassium administration reduced plasma renin activity in 18 of 28 studies of both normal and hypertensive subjects. Suppression of renin often occurred despite sodium diuresis induced by potassium administration. The renin suppression was related to induced changes in plasma potassium concentration and urinary potassium excretion. The failure of suppression of plasma renin in 10 studies could be accounted for by the smaller amounts of potassium administered to these subjects, together with a possibly overriding influence of an induced sodium diuresis. In six studies potassium deprivation invariably increased plasma renin activity even though a tendency for sodium retention often accompanied this procedure. The data indicate that both the suppression of plasma renin activity induced by potassium administration and the stimulation of renin activity which follows potassium depletion occur independently of associated changes in either aldosterone secretion or in sodium balance. However, the results do suggest that in various situations, the influence of potassium on plasma renin activity may be either amplified or preempted by changes in sodium balance. These interactions between potassium and plasma renin could be mediated by an ill-defined extrarenal pathway. But the findings are more consistent with an intrarenal action of potassium ions to modify renin release. Potassium might modify renin secretion directly by acting on the juxtaglomerular cells or by a change in its tubular reabsorption or secretion. The effects of potassium ions on renin secretion might also be mediated indirectly via an induced change in tubular sodium transport.
Adult↗
Serum potassium level and dietary potassium intake as risk factors for stroke.
BACKGROUND: Numerous studies have found that low potassium intake and low serum potassium are associated with increased stroke mortality, but data regarding stroke incidence have been limited. Serum potassium levels, dietary potassium intake, and diuretic use in relation to risk for stroke in a prospectively studied cohort were investigated. METHODS: The study comprised 5,600 men and women older than 65 years who were free of stroke at enrollment. Baseline data included serum potassium level, dietary potassium intake, and diuretic use. Participants were followed for 4 to 8 years, and the incidence and types of strokes were recorded. Low serum potassium was defined as less than 4.1 mEq/L, and low potassium intake as less than 2.4 g/d. RESULTS: Among diuretic users, there was an increased risk for stroke associated with lower serum potassium (relative risk [RR]: 2.5, p < 0.0001). Among individuals not taking diuretics, there was an increased risk for stroke associated with low dietary potassium intake (RR: 1.5, p < 0.005). The small number of diuretic users with lower serum potassium and atrial fibrillation had a 10-fold greater risk for stroke compared with those with higher serum potassium and normal sinus rhythm. CONCLUSIONS: A lower serum potassium level in diuretic users, and low potassium intake in those not taking diuretics were associated with increased stroke incidence among older individuals. Lower serum potassium was associated with a particularly high risk for stroke in the small number of diuretic users with atrial fibrillation. Further study is required to determine if modification of these factors would prevent strokes.
Aged↗
Internal potassium balance and the control of the plasma potassium concentration.
The plasma potassium concentration is determined both by external potassium balance and by the distribution of potassium between extracellular and intracellular fluid compartments, i.e., "internal potassium balance." Whenever external potassium balance is altered, the resultant change in the plasma potassium concentration is strongly influenced by concomitant alterations in internal potassium balance. Several factors alter internal potassium balance independently of changes in external balance. Acid-base disturbances produce shifts of potassium into or out of cells, but attempts to quantify these effects are not likely to be clinically useful. Hypertonicity produces a shift of potassium out of cells. Several hormones (insulin, aldosterone, catecholamines, glucagon, and growth hormone) may have roles in internal potassium balance. Digitalis and succinylcholine, by producing efflux of potassium from cells, may cause hyperkalemia. Potassium is released from skeletal muscle during exercise, causing an increase in the plasma potassium concentration. The periodic paralyses are associated with well-defined transient alterations in internal potassium balance.
Acid-Base Imbalance↗
Dietary potassium modulates active potassium absorption and secretion in rat distal colon.
To determine the effect of variations in body stores of potassium on the rate of active potassium transport in the large intestine, unidirectional 42K fluxes were performed under short-circuit conditions across isolated distal colonic mucosa of control, dietary potassium-depleted and dietary potassium-loaded rats. Potassium depletion stimulated net potassium absorption (JK net) (0.87 +/- 0.19 vs. 0.49 +/- 0.04 mu eq X h-1 X cm-2, P less than 0.025) due to a 40% increase in mucosal-to-serosal potassium transport (JK m----s). In sodium-free Ringer solution JK net in the potassium-depleted group was also significantly greater than in controls (1.93 +/- 0.26 vs. 1.01 +/- 0.11 mu eq X h-1 X cm-2, P less than 0.005). In contrast, in chloride-free Ringer solution JK net was identical in the control and potassium-depleted groups (0.39 +/- 0.05 vs. 0.46 +/- 0.07 mu eq X h-1 X cm-2, P = NS). Potassium loading reversed net potassium absorption to net potassium secretion (-0.76 +/- 0.08 mu eq X h-1 X cm-2, P less than 0.001) as the result of a decrease in JK m----s and an increase in serosal-to-mucosal potassium transport (JK s----m). Net potassium secretion was abolished in the absence of either sodium or chloride from the bathing solution but not by mucosal amiloride. In sodium-free Ringer solution JK net was similar in control and potassium-loaded groups, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
Amiloride↗
Potassium transport by the renal distal tubule: effects of potassium loading.
Microperfusion studies were performed on superficial distal tubules to determine the relationship between potassium secretion by the distal tubule and plasma potassium concentrations in rats on a control and a high potassium diet. Potassium was infused in graded doses into animals on a control diet and into animals receiving a high potassium diet. Since potassium loading in rats is known to inhibit proximal tubular sodium and fluid reabsorption and thereby could lead to nonspecific flow-related stimulation of potassium secretion by the distal tubule, continuous microperfusion techniques at constant flow rate were used to measure the rate of potassium secretion. Additionally, plasma aldosterone levels were measured and renal clearance experiments carried out. The results show that potassium secretion, restricted to cells of the late distal tubule, reaches a maximal rate at a plasma potassium concentration of about 6 meq/liter. Potassium adaptation significantly enhances potassium secretion compared with animals on a control diet over a range of plasma potassium from 3.8 to 7.4 meq/liter. Enhanced potassium secretion by the distal tubule, in both control and potassium-adapted animals, is associated with increased aldosterone levels.
Aldosterone↗
Potassium toxicity and acid-base balance from large oral doses of potassium to young calves.
Potassium chloride and sodium chloride were infused into the reticulorumen of male Holstein calves, approximately 6 mo of age and 260 kg, at .29, .58, 1.15, 1.73, 2.31, or 2.88 g potassium per kilogram body weight or 1.35, 2.12, or 2.16 g sodium per kilogram in equal volumes of water. Paired controls were infused with water. Calves were monitored for physiological changes for 6 h at 15, 30, or 60-min intervals. Potassium and total solids of plasma and packed cell volume were increased at potassium doses greater than .29 g of potassium per kilogram body weight within 1 h after dosing. At the higher doses of potassium, sodium content of plasma increased about 1 h after the increase in plasma potassium. Respiration rates within a potassium treatment varied with respect to time after dosing, but generally they increased, and associated variables of carbon dioxide pressure, pH, and bicarbonate in blood were decreased accordingly. Clinical toxicity signs, including excess salivation, muscular tremors of legs, and excitability were observed with potassium doses greater than .58 g of potassium per kilogram body weight. Three of five calves given 1.73 g of potassium per kilogram, three of four calves given 2.31 g of potassium per kilogram, and one calf given 2.88 g of potassium per kilogram body weight died. With a small number of calves, oral sodium infusions increased plasma sodium in proportion to the dose, but plasma potassium remained relatively constant. Sodium infusions of 2.12 and 2.16 g of sodium per kilogram body weight were fatal.
Acid-Base Imbalance↗
The electrical basis for enhanced potassium secretion in rat distal colon during dietary potassium loading.
Previous studies in rat distal colon provide evidence for an active absorptive process for potassium under basal conditions, and for active potassium secretion during chronic dietary potassium loading. The present studies were performed with conventional and potassium-selective microelectrodes to determine the electrical basis for the increase in transcellular (active) potassium secretion observed during potassium loading. Compared to control tissues, potassium loading resulted in a 5-fold increase in transepithelial voltage (VT) and a 52% decrease in total resistance (RT) in the distal colon. The rise in VT was due to a decrease in apical membrane resistance and an increase in basolateral membrane voltage from -45 +/- 2 mV (cell interior negative) in control to -56 +/- 2 mV (p less than 0.001) in potassium loaded tissues. This difference in basolateral membrane voltage reflected in increase in intracellular potassium activity from 86 +/- 4 mM to 153 +/- 12 mM (P less than 0.001). In control tissues, the sequential mucosal addition of the sodium channel blocker amiloride (0.1 mM) and the potassium channel blocker tetraethylammonium chloride (TEA: 30 mM) produced no effect on the electrical measurements. However, in potassium loaded tissues, amiloride and TEA produced transepithelial changes consistent with inhibition of apical membrane conductances for sodium and potassium, respectively, reflected by increases in the resistance ratio, alpha (ratio of apical to basolateral membrane resistances). These data indicate that the decrease in apical membrane resistance during potassium loading was caused by an increase in apical membrane conductance for both potassium and sodium.
Amiloride↗
Potassium supplements and potassium-sparing diuretics. A review and guide to appropriate use.
Epidemiological and clinical studies suggest that low dietary potassium intake may have an important role in determining the development of diseases such as hypertension, and perhaps even stomach cancer, and that increased potassium intake may have beneficial effects in several other conditions. Dietary adjustment or active potassium supplementation has been suggested as a natural, less costly and safe method of increasing potassium levels, although active supplementation with tablets or solutions is not recommended in healthy people with normal serum potassium levels. However, increasing dietary potassium intake in the elderly and in patients with renal impairment must be considered with caution. Diuretics have a long established role in the management of hypertension and heart failure. There is no convincing evidence to suggest that the small reduction in plasma potassium levels associated with low dose thiazide and loop diuretic therapy needs to be routinely prevented by the use of potassium-sparing drugs. In non-digitalised patients little association has been found between mild diuretic-induced hypokalaemia and arrhythmias. Thus, the routine prophylactic use of potassium-sparing diuretics in combination with non-potassium-retaining diuretics for the treatment of hypertension and oedematous states is not justified. Based on current evidence, treating all patients whose serum potassium level decreases below 3 mmol/L is recommended, although for certain patients at particular risk of hypokalaemia, levels may need to be maintained above 3.5 mmol/L. In overt hypokalaemia, several therapeutic options are available to the clinician. These include increased consumption of potassium-rich foods, the use of salt substitutes, medicinal potassium supplementation or distal tubular (potassium-sparing) diuretics.
Administration, Oral↗
Potassium and sodium transport along the loop of Henle: effects of altered dietary potassium intake.
We assessed the effects of changes in potassium (K+) balance on the function of the loop of Henle by a combination of renal clearance and microperfusion experiments. Rat superficial cortical nephrons were perfused in vivo at 20 nl.min-1 from late proximal to early distal tubule with an artificial end-proximal solution containing either 3.8 or 1.8 mM potassium. Rats were fed a control diet, a low-potassium diet for at least three weeks, or a high-potassium diet for 10 to 14 days. When compared with the appropriate end-proximal potassium concentration in the perfusion fluid, potassium absorption along the loop of Henle (JK) increased in potassium-depletion whereas sodium (JNa) and fluid (Jv) absorption decreased. In rats fed a high-potassium diet, absorption of potassium, sodium and fluid was depressed. We propose that changes of external potassium balance affect the transport of electrolytes and fluid along the loop of Henle in vivo by modulating the transport of potassium and sodium primarily in the thick ascending limb. Changes in potassium reabsorption may also be affected by alterations of potassium-recycling.
Animals↗
Studies of the control of plasma aldosterone concentration in normal man. II. Effect of dietary potassium and acute potassium infusion.
The responses of plasma aldosterone, cortisol, and corticosterone to an infusion of 75 mEq of potassium chloride over 120 min were studied in 10 normal subjects. Five subjects were fed a 10 mEq and five a 200 mEq sodium diet, while all subjects ingested 40 mEq and 200 mEq potassium sequentially. Two potassium infusions were performed in each subject when in balance on a fixed sodium intake and low and then high potassium diets. Regardless of dietary intake, increases of serum potassium of 0.5-1.5 mEq/liter above preinfusion levels were usually associated with significant increments in plasma aldosterone concentration. Our data agree with previous evidence that the potassium ion stimulates the adrenal cortex directly to secrete aldosterone. Peripheral renin activity did not increase after the potassium infusion. Plasma cortisol and corticosterone levels generally followed the expected diurnal decline during the infusion, implying that ACTH secretion did not increase. The plasma aldosterone response to incremental changes in serum potassium was linear on each of the four diets. The slopes of these linear relationships increased significantly when the potassium intake was increased from 40 to 200 mEq. No increase in slope occurred on either potassium intake when dietary sodium was restricted from 200 to 10 mEq. Thus, identical increases in serum potassium were associated with greater increments in plasma aldosterone above preinfusion levels on either sodium intake when the 200 mEq potassium diet was compared with the 40 mEq potassium intake.
Adrenal Glands↗
Chronic potassium supplementation of newborn dogs increases cortical Na,K-ATPase but not urinary potassium excretion.
The distal nephron of the newborn dog cannot secrete an acute potassium load as efficiently as can that of the adult dog. Distal nephron potassium secretion is dependent upon basolateral Na,K-ATPase activity. Because Na,K-ATPase activity is lower in the immature than the mature distal nephron, it was hypothesized that lower Na,K-ATPase activity may be responsible for the lower potassium secretory capacity of the immature nephron. In the adult, chronic high dietary potassium intake increases renal tubular potassium secretory capacity by increasing Na/K pump abundance in distal nephron segments responsible for potassium secretion. Therefore, in order to test the above hypothesis, renal cortical and outer medullary Na,K-ATPase activity under Vmax conditions (a measure of pump abundance) and urinary potassium excretion during acute potassium loading were determined in 7 age-matched, litter mate pairs (chronically potassium supplemented versus control) newborn dogs. The potassium supplemented member of each pair received 6 mmol.day-1.kg-1 of KCl as a 150 mM solution for 7-21 days after birth and the control member received an equal volume of water for the same period of time. This protocol resulted in a doubling of renal cortical Vmax Na,K-ATPase activity in the potassium supplemented animals (from 369 +/- 186 to 718 +/- 286 nmol Pi liberated.h-1.micrograms DNA-1, P = 0.025). There was no significant change in outer medullary enzyme activity. Contrary to the above hypothesis, this increase in cortical enzyme activity was not associated with increased potassium excretion at baseline or during acute potassium loading.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Relationships between serosal medium potassium concentration and sodium transport in toad urinary bladder. I. Effects of different medium potassium concentrations on electrical parameters.
When serosal medium potassium was decreased from the usual concentration of 3.5 mM, the short-circuit current (SCC) of hemibladders in chambers immediately and transiently increased. The maximum SCC attained was greater the greater the decrease in serosal potassium, and was twice the initial SCC when the final serosal medium was potassium-free. The SCC then fell to its previous level for final serosal potassium concentrations greater than 2 mM and to less than its previous level for those less than 2 mM, being lowest (15% of previous levle) in potassium-free sodium Ringer's. When serosal medium potassium was increased from 3.5 mM by substituting potassium for sodium, SCC transiently decreased and then recovered to its previous level. Steady SCC was the same in serosal media of 2-116 mM potassium; conductance increased and p.d. decreased after incubation in 50-116 mM potassium serosal media. Short-circuit current and p.d. transiently increased (decreased) whenever serosal medium potassium was decreased (increased); conductance increased with any change in serosal potassium. Changing mucosal medium potassium concentration between 0 and 50 mM did not affect SCC. The initial transient increase and subsequent decrease in SCC on removing serosal potassium were partially prevented by 3.5 mM rubidium or caesium, or by 116 mM choline in the serosal medium. The transient changes in SCC were due partly to changes in transepithelial sodium transport.
Animals↗
The relation between potassium in body fluids and total body potassium in healthy and diabetic subjects.
1. The concentration of potassium in the erythrocytes and the plasma of forty-one normal subjects and twenty-five diabetic patients was measured and the results were used to calculate the total amount of potassium in the erythrocyte mass and the total amount of potassium in the plasma. The total body potassium was measured in a whole-body monitor. 2. In normal subjects a close correlation was found between total erythrocyte potassium and total body potassium and also between total plasma potassium and total body potassium. 3. The regression relation between total body potassium and total erythrocyte potassium in normal subjects was used to predict the total body potassium in diabetic patients. There was reasonable agreement between the measured and predicted total body potassium but there was poor agreement between the measured total body potassium and that predicted from the patient's height and age or height and age or height, weight and age.
Adult↗
Effect of extracellular potassium on the transport of sodium and potassium in rat thymocytes.
1. The effect of extracellular potassium on the transport of sodium and potassium in rat thymocytes has been studied in vitro. 2. A significant increase in the rate constant for total and ouabain-sensitive sodium efflux was demonstrated at an extracellular potassium concentration of 1 mmol/l as compared with that at either 0 or 2 mmol/l. 3. At potassium concentrations below 3 mmol/l ouabain-sensitive sodium influx was observed suggesting sodium-sodium exchange catalysed by the sodium pump. 4. Both total and ouabain-insensitive potassium efflux rose with external potassium. A small ouabain-sensitive potassium efflux was observed at all levels of external potassium studied. 5. Total and ouabain-insensitive potassium influx increased with external potassium, but did not appear to saturate. Ouabain-sensitive potassium influx reached a maximum at an external potassium concentration of 2 mmol/l then decreased with increasing external potassium.
Animals↗