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PubMed1980

The equilibrium between different conformations of the unphosphorylated sodium pump: effects of ATP and of potassium ions, and their relevance to potassium transport.

1. Changes in the intrinsic fluorescence of Na, K-ATPase protein have been used to monitor the interconversion of E(1) (low fluorescence) and E(2) (high fluorescence) forms of the unphosphorylated enzyme.2. In media lacking sodium and nucleotides, 1 mM-potassium was sufficient to convert practically all of the enzyme into the E(2) form. In media containing 1 mM-potassium, 1 mM-EDTA, and no sodium or magnesium, the addition of ATP, or its beta, gamma-imido or methylene analogues, converted the enzyme back into the E(1) form. The relation between nucleotide concentration and the fraction of the enzyme that was in the E(1) form could be described by a rectangular hyperbola, with a K((1/2)) of about 15 muM for ATP, 65 muM for adenylyl-imidodiphosphate (AMP-PNP) and 180 muM for adenylyl (beta, gamma-methylene)-diphosphonate (AMP-PCP). ADP also converted the enzyme back into the E(1) form, with a K((1/2)) of about 25 muM, but the relation between concentration and fraction converted was not well described by a rectangular hyperbola.3. In similar media containing 50 mM-potassium, much higher concentrations of ATP were required to convert the enzyme back into the E(1) form, and the conversion was probably incomplete.4. If we assume that ATP and potassium ions affect each other's binding solely by altering the equilibrium between E(1) and E(2) forms of the enzyme, we are able to conclude (i) that potassium ions bind to the E(1) form with a moderately low affinity, (ii) that, in the absence of nucleotides, the equilibrium between E(1)K and E(2)K is poised strongly in favour of E(2)K, (iii) that the binding of ATP to a low-affinity site alters the equilibrium constant for the interconversion of E(1)K and E(2)K by two to three orders of magnitude, so that, at saturating levels of ATP, the equilibrium is probably slightly in favour of E(1)K, and (iv) that in sodium-free, potassium-containing media, ATP will appear to bind to the enzyme more tightly than would be expected from the dissociation constant of the E(2)K. ATP complex.5. The pattern of the equilibrium constants for the various reactions between E(1), E(2), ATP and potassium is compatible with the hypothesis that the ATP-accelerated conversion of E(2)K into E(1)K, and the subsequent release of potassium ions from low-affinity inward-facing sites, are part of the normal sequence of events during potassium influx in physiological conditions.

Adenosine Diphosphate↗
PubMed1987

Independent effects of aldosterone and potassium on induction of potassium adaptation in rat kidney.

We examined the independent effects of a high potassium diet and increased aldosterone levels on the development of renal potassium adaptation. This condition is defined by the increased ability of the kidneys to excrete an acute infusion of potassium. Rats were adrenalectomized (ADX) and received aldosterone at basal levels (0.5 microgram/100 g X d) or at high levels (2.0 micrograms/100 g X d) for 10 d. In each experimental group, animals received either a control diet or a high potassium diet. In ADX animals with basal aldosterone levels, a high potassium intake increased but did not completely restore the ability to excrete potassium and induced proliferation of the basolateral membrane of principal cells in the collecting tubule (i.e., morphologic adaptation). In contrast, increased aldosterone did not induce functional adaptation. Elevated aldosterone and dietary potassium intake were required to produce functional potassium adaptation indistinguishable from that in potassium-loaded, adrenal-intact animals.

Adaptation, Physiological↗
PubMed1989

[Role of prostanoids in the control of renal function in normal potassium balance and in acute experimental potassium depletion. 4. Relation of extrarenal parameters, renal function parameters and urinary excretion of prostanoids].

The renal function has been evaluated by clearance (cl.) method during hypotonic polyuria and successive moderate antidiuresis induced by a low dose of lysine-8-vasopressin; four 15 min and two 60 min cl. periods were performed, respectively. Glomerular filtration rate was estimated by creatinine cl.; the osmotic cl. (Cosm, CH2O), the absolute and fractional excretions of water, sodium, potassium and chloride were determined by usual methods. The urinary concentrations of PGE2, 6-keto-PGF1 alpha (6KPGF) and TxB2 were measured by RIA. The study protocol was applied in normal potassium balance and experimental potassium balance (KD), both in absence and presence of indomethacin. In KD groups with a potassium cumulative deficit of 198.4 +/- 22.2 meq (D3; n = 6) during polyuria significant correlations are consistent with the hypothesis that the lower the plasma potassium concentration is the higher the urinary chloride excretion and the inhibition of distal fractional chloride reabsorption. Moreover, by utilizing the polyuria and antidiuresis data pool, the effects of urine flow rate changes on PGE2 and 6KPGF urinary excretions are blunted as compared to normal potassium balance (n = 14). After indomethacin treatment (D3.I) the following functional relationships are disclosed: a) the lower the kaliemia is the lower the urinary chloride and potassium excretions and the higher the fractional isosmotic reabsorption; b) the lower the urinary potassium excretion is the lower the urinary chloride excretion. In both D3 and D3.I experimental groups the positive correlation between urinary chloride excretion and urinary potassium excretion is significant.

6-Ketoprostaglandin F1 alpha↗
PubMed1964

TRACER AND NON-TRACER POTASSIUM FLUXES IN FROG SARTORIUS MUSCLE AND THE KINETICS OF NET POTASSIUM MOVEMENT.

Experiments were performed to test the applicability of permeability kinetics to whole frog sartorius muscle using K(42) ions as tracers of potassium flux. The whole muscle was found to obey closely the kinetic laws expected to hold for single cellular units in which the potassium fluxes are membrane-limited and intracellular mixing is rapid enough not to introduce serious error. In a 5 mM K Ringer's solution, potassium efflux was very nearly equal to influx when the rate constant for K(42) loss was applied to the whole of the muscle potassium. Over a fairly wide range of external potassium concentration, the assumed unidirectional fluxes measured with tracer K(42) showed good agreement with net potassium changes determined analytically. The specific activity of potassium lost from labeled muscles to an initially K-free Ringer's solution was measured as a test of the adequacy of intracellular mixing. The results were those expected for a population of cells with uniformly distributed intracellular K(42). A small deviation was encountered which can be attributed either to a dispersion of fiber sizes in the sartorius or to a possible small additional cellular compartment in each individual fiber. The additional cellular compartment, should it exist, contains from 0.5 to 1 per cent of the muscle potassium. This is evidently not large enough to interfere seriously with the applicability of permeability kinetics to the whole muscle.

Animals↗
PubMed1989

The effect of potassium and potassium plus magnesium supplementation on ventricular extrasystoles in mild hypertensives treated with hydrochlorothiazide.

Eleven mild hypertensives with base-line ventricular extrasystoles underwent a 24-week period of treatment with hydrochlorothiazide 50 mg daily. After 8 weeks of treatment either potassium as hydrochloride 1 g twice daily, or a combination of potassium hydrochloride 1 g and magnesium hydroxide 500 mg twice daily was added to the diuretic therapy in a randomised, double-blind, cross-over design. Each treatment period lasted 8 weeks. Supplementation with potassium or potassium plus magnesium resulted in a clear trend for suppression of ventricular ectopic activity. There was no difference in ventricular extrasystoles between the two supplementation groups. Supplementation with potassium plus magnesium but not with potassium only, resulted in a significant rise in serum potassium values (P less than 0.01). Our study suggests that potassium should be supplemented in thiazide-treated hypertensives who are prone to develop ventricular extrasystoles. Addition of magnesium to potassium supplementation does not result in further improvement in ventricular ectopic suppression.

Adult↗
PubMed1995

[Potassium citrate versus potassium chloride in essential hypertension. Effects on hemodynamic, hormonal and metabolic parameters].

A study was conducted on 25 patients (18 men, seven women; mean age 48 [24-70] years) with essential hypertension (EH) to see whether an increase in potassium supply influences blood pressure as well as metabolic and hormonal parameters, and whether the anion administered together with potassium affects the results. In a randomized, cross-over trial sequence the patients daily received 120 mmol potassium chloride, 120 mmol potassium citrate or a placebo, each for 8 weeks. Between each of the three periods there was a "wash-out" phase of 4 weeks each. After 8 weeks of potassium citrate intake the systolic and diastolic pressures were reduced significantly, by a mean of 6.2/3.8 mm Hg (P < 0.05). But after potassium chloride there was only a small, not significant, reduction. Metabolic and hormonal parameters (fasting glucose concentration, glucose tolerance test, lipid electrophoresis; plasma renin activity, plasma concentration of aldosterone, noradrenaline and insulin) were not significantly changed.--These findings suggest that an increased supply of potassium has a favourable haemodynamic effect, but this varies markedly between different potassium salts. An increase in potassium supply should thus be considered as an additional measure in the treatment of EH. As long as renal function is normal no unfavourable metabolic effect need be feared.

Adult↗
PubMed1994

Do potassium channel openers compete with ATP to activate ATP sensitive potassium channels?

Potassium channel openers are a class of chemically heterogeneous compounds that produce vasodilatation by opening vascular smooth muscle potassium channels. Using various configurations of the powerful patch clamp technique, the molecular pharmacology of potassium channel openers has been largely explored in different cellular systems. These studies have revealed that the primary molecular target for potassium channel openers is this class of potassium channel proteins that close under the influence of intracellular ATP and have thus been named ATP sensitive potassium channels. Direct recordings of unitary ATP sensitive potassium channels in cell detached membrane patches support the view that potassium channel openers compete with intracellular ATP to prevent channel inhibition. However, there also exists experimental evidence that contradicts the competition hypothesis and suggests the involvement of phosphorylation-dephosphorylation mechanisms. The aim of the present article is to review experimental data that support, or inversely, contradict the potassium channel opener-ATP competition theory.

Adenosine Triphosphate↗
PubMed1973

Modulation of plasma aldosterone concentration by plasma potassium in anephric man in the absence of a change in potassium balance.

In studies on seven anephric patients, glucose and insulin administration before hemodialysis produced a significant reduction in plasma potassium concentration (mean reduction = 1.3, 1.7, and 1.4 meq/liter at 60, 120, and 180 min, respectively) which was accompanied by a significant and sustained reduction in plasma aldosterone concentration. There was a significant correlation between plasma aldosterone and plasma potassium concentration (r = +0.74, P < 0.001) and between changes in the concentration of plasma aldosterone occurring in individual patients and the corresponding changes in plasma potassium concentration (r = +0.52, P < 0.01). There was no significant change in plasma sodium concentration, and plasma corticoid concentration, which was monitored as an index of ACTH elaboration, was reduced at 60 min but increased subsequently as symptoms attributable to hypoglycemia were observed. These studies demonstrate that plasma aldosterone concentration can be modulated acutely by transitory changes in plasma potassium concentration without a change in potassium balance. The effect of glucose and insulin administration on intracellular potassium in the adrenal cortex is uncertain, and although increased net movement of potassium into cells is the presumptive mechanism of the reduction in plasma potassium concentration, whether the potassium content of the adrenal cortex may have increased or decreased or remained essentially unchanged, cannot be inferred from our data.

Aldosterone↗
PubMed1982

Bioequivalence of a slow-release potassium tablet and a liquid potassium supplement.

The rate and extent of potassium absorption from a slow-release potassium chloride tablet and a 10% potassium chloride solution were compared in 12 healthy male volunteers, 18-25 years old. A single 48 mEq potassium dose of the tablet released potassium 30 min slower than the same dose of potassium chloride solution. Potassium was completely absorbed from both preparations within 24 h. Complete absorption was confirmed by quantitative determination of fecal potassium excretion. Gastrointestinal tolerance was good with both preparations, although the incidence of adverse experiences was slightly higher with the liquid preparation. "Bad taste" was not associated with the slow-release tablet; 92% of the subjects reported "bad taste" with the potassium chloride solution.

Adolescent↗
PubMed1997

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

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

Animals↗
PubMed1999

A secretory mechanism of renal kallikrein by a high potassium ion; a possible involvement of ATP-sensitive potassium channel.

A relatively rapid excretion of urinary kallikrein into urine was observed by an intravenous infusion of high potassium in anesthetized rats. Superfusion of sliced cortex isolated from rat kidney with an isotonic solution containing more than 20 mM of KCl significantly stimulated the release of kallikrein. The latter in vitro result supported another mechanism for the release of renal kallikrein from kidney other than biosynthesis of kallikrein by aldosterone released from adrenal cortex after loading of high potassium and the mechanism was elucidated. ATP-sensitive potassium channel blockers, glibenclamide, 4-morpholinecarboximidine-N-1-adamantyl-N'-cyclohexylhydr ochloride (U37883A), and barium chloride, which inhibit an efflux of intracellular potassium to block the channel, showed a significant increase of the kallikrein release from the slice of kidney cortex. Cytochalasin B, which inhibits a polymerization of actin, also showed a stimulation of the release. Enhanced release of kallikrein by a high potassium or ATP-sensitive potassium channel blocker was reduced by the absence of calcium ion and the presence of voltage-dependent calcium channel blocker in the superfused solution. These results indicate the ATP-sensitive potassium channel which couples to voltage-dependent calcium channel and cytoskeletal protein could be involved in a rapid secretory mechanism of renal kallikrein by high potassium.

ATP-Binding Cassette Transporters↗
PubMed1999

Early increases in renal kallikrein secretion on administration of potassium or ATP-sensitive potassium channel blockers in rats.

1 This study aimed to examine whether administration of potassium or ATP-sensitive potassium channel (KATP channel) blockers caused early increases in renal kallikrein (KK) secretion. To clarify this mechanism, the effect on renal KK secretion of a KATP channel blocker was compared with the effect resulting from use of an osmotic diuretic or volume load. Furthermore, the effect on potassium-induced increases in renal KK secretion by an additional treatment using a KATP channel blocker was examined. Lastly, the effect of a KATP channel blocker on renal KK secretion was also examined in superfused slices of kidney cortex. 2 Intravenous infusion of potassium augmented renal KK secretion within 30 min while urine volume increased gradually in both the potassium loading and control groups. 3 Administration of the KATP channel blocker, 4-morpholinecarboximidine-N-1-adamantyl-N'-cyclohexylhydr ochloride (PNU-37883A) or glibenclamide, caused a dose-dependent increase in renal KK secretion. 4 The concentration of KK in urine was higher in the PNU-37883A group as compared to the osmotic-diuretic or volume-load group. 5 PNU-37883A had no additive effect on the potassium-induced increase in renal KK secretion. 6 Renal KK secretion increased in slices of kidney cortex incubated with PNU-37883A within 10 min of superfusion. 7 In conclusion, administration of both potassium and KATP channel blockers induced early increases in renal KK secretion in the absence of the washout phenomenon. Potassium loading may have increased renal KK secretion through the same mechanism as the KATP channel blocker.

Adamantane↗
PubMed1999

Modulation of jellyfish potassium channels by external potassium ions.

The amplitude of an A-like potassium current (I(Kfast)) in identified cultured motor neurons isolated from the jellyfish Polyorchis penicillatus was found to be strongly modulated by extracellular potassium ([K(+)](out)). When expressed in Xenopus oocytes, two jellyfish Shaker-like genes, jShak1 and jShak2, coding for potassium channels, exhibited similar modulation by [K(+)](out) over a range of concentrations from 0 to 100 mM. jShak2-encoded channels also showed a decreased rate of inactivation and an increased rate of recovery from inactivation at high [K(+)](out). Using site-directed mutagenesis we show that inactivation of jShak2 can be ascribed to an unusual combination of a weak "implicit" N-type inactivation mechanism and a strong, fast, potassium-sensitive C-type mechanism. Interaction between the two forms of inactivation is responsible for the potassium dependence of cumulative inactivation. Inactivation of jShak1 was determined primarily by a strong "ball and chain" mechanism similar to fruit fly Shaker channels. Experiments using fast perfusion of outside-out patches with jShak2 channels were used to establish that the effects of [K(+)](out) on the peak current amplitude and inactivation were due to processes occurring at either different sites located at the external channel mouth with different retention times for potassium ions, or at the same site(s) where retention time is determined by state-dependent conformations of the channel protein. The possible physiological implications of potassium sensitivity of high-threshold potassium A-like currents is discussed.

Amino Acid Sequence↗
PubMedDate not supplied

Histochemical localization of phosphatases in the pig placenta: II. Potassium-dependent and potassium-independent p-nitrophenyl phosphatases at high pH; relation to sodium-potassium-dependent adenosine triphosphatase.

Histochemical localization by Mg2+ capture methods of K+-dependent, ouabain-sensitive phosphatase activity in the pig placenta shows that strong Na+,K+-dependent adenosine triphosphatase (Na+,K+-ATPase) activity is restricted to the basal zone of the columnar epithelium covering the areolar chorionic villi. It is proposed that active Na+ absorption at this epithelium may be the source of the ouabain-sensitive, fetal-side-positive potential difference which can be measured across the placental membrane in vitro. The one-step procedure for Na+,K+-ATPase localization is unsatisfactory in this organ as any specific ATPase reaction is swamped by activity probably attributable to uteroferrin and other non-specific phosphatases.

4-Nitrophenylphosphatase↗
PubMed1976

The effects of ouabain and ethacrynic acid on the intracellular sodium and potassium concentrations in renal medullary slices incubated in cold potassium-free ringer solution and re-incubated at 37 degrees C in the presence of external potassium.

1. The cells in slices cut from the renal outer medulla of normally hydrated adult rats were loaded with Na and depleted of K by incubation for up to 100 min in cold iso-osmolal K-free Ringer containing 180 mM-Na. There was a continuous net cellular water loss during this time; an inverse linear relationship existed between water content and intracellular Na concentration. 2. The original intracellular Na and K concentration were restored following 60 min re-incubation in warm Ringer (37 degrees C) containing 5-9 mM-K. Restoration of cellular water content was incomplete after re-incubation for up to 120 min. 3. During incubation in cold K-free Ringer the presence of 1 mM ouabain did not affect cellular Na uptake or K and water loss. Ethacrynic acid, 1 mM, completely blocked cellular Na uptake and water loss, without affecting the intracellular K concentration at 100 min. When ouabain and ethacrynic acid were present together water loss was also prevented but intracellular Na concentration rose slightly by 100 min. 4. During re-incubation in warm K-containing Ringer 1 mM ouabain inhibited Na extrusion completely for up to 60 min while only partially preventing K uptake and further depressing the level of cellular hydration. Ouabain in the presence of 1 mM ethacrynic acid had similar effects on intracellular Na and K concentrations, but raised the level of intracellular water above that of cells in control slices. 5. Ethacrynic acid alone, 1 mM, did not interfere with Na extrusion or K uptake, but also raised intracellular water above control values. 6. The results obtained are discussed in relation to (a) the nature of the preparation used, (b) the possible membrane transport processes occurring and their known or suggested sensitivity to ouabain and ethacrynic acid, (c) the mechanisms which may be responsible for cell volume maintenance in the medulla.

Animals↗
PubMed1981

Mechanistic implications of the potassium-potassium exchange carried out by the sodium-potassium pump.

1. The magnitude of the K-K exchange carried out by the Na pump in human red cells was measured as a function of the external K concentration in cells with high and low intracellular K. The apparent K1/2 for external K and the Vm increased by the same proportion when intracellular K was raised. The result suggests that the K-K exchange is part of a ping-pong reaction mechanism. 2. The velocity of the exchange increases monotonically with intracellular phosphate and ATP concentration; neither substrate inhibits at very high concentration. 3. These results seem to require that the enzyme species which carries out the exchange is both phosphorylated and combined with ATP.

Adenosine Triphosphate↗