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At least 235 records · Page 13Linked to original sources
PubMed1994

Pretreatment with the adenosine triphosphate-sensitive potassium channel opener nicorandil and improved myocardial protection during high-potassium cardioplegic hypoxia.

We hypothesized that pretreatment with the potassium channel opener nicorandil might enhance myocardial protection achieved by cold (20 degrees C) high-potassium (16 mmol/L) cardioplegia (5 ml/min) during long-duration (120 minutes) myocardial hypoxia (average oxygen content 5.4 ml/dl). We tested a 15-minute infusion of nicorandil (1 mmol/L) given only before (group A, n = 8) or before and during cardioplegia (group B, n = 8) in guinea pig papillary muscle preparations contracting isometrically while stimulated (4 mA, 2 msec) at 1600 msec cycle length. Nicorandil was significantly negative inotropic before cardioplegia and shortened significantly action potential duration. During cardioplegia, time to arrest of contraction was shortened from 145 +/- 28 seconds (mean +/- standard error) in the vehicle group (dimethyl sulfoxide 1:100; n = 8) to 56 +/- 10 seconds (p < 0.02) and 68 +/- 5 seconds (p < 0.05) in groups A and B, respectively. Recovery of developed tension at 60 minutes of normothermic reoxygenation (expressed as percent of prehypoxia basal value) was ameliorated from 54% +/- 6% (vehicle group) to 92% +/- 4% (group A, p < 0.01) and to 119% +/- 19% (group B, p < 0.01). The specific potassium channel blocker glibenclamide (glib: 1 mumol/L, n = 8) prolonged action potential duration and was without effect on time to arrest. On reoxygenation, the glib group had prolonged time to half relaxation (versus group A, p < 0.02) and the worst percent developed tension at 60 minutes (40% +/- 4%). In the overall study, time to arrest and percent developed tension at 60 minutes were inversely correlated (r = -0.45, p < 0.01). Arrhythmias were never observed. Multivariate analysis showed that pretreatment with nicorandil (with or without drug adjunct to cardioplegic solution) was a significant factor (r2 = 0.65, p = 0.0001) to influence reoxygenation-mediated recovery of mechanical function. Neither the negative inotropic effect of nicorandil before cardioplegia nor its abbreviating action on time to arrest during cardioplegia was contributory to explain recovery of function on reoxygenation. In subgroup analysis, negative inotropism and the shortening of action potential duration were contributory factors. These data suggest that nicorandil pretreatment activates potassium channels and enhances the myocardial protection provided by cold cardioplegia an effect, which is evident after a long hypoxic period, late on reoxygenation.

Action Potentials↗
PubMed2000

New guidelines for potassium replacement in clinical practice: a contemporary review by the National Council on Potassium in Clinical Practice.

This article is the result of a meeting of the National Council on Potassium in Clinical Practice. The Council, a multidisciplinary group comprising specialists in cardiology, hypertension, epidemiology, pharmacy, and compliance, was formed to examine the critical role of potassium in clinical practice. The goal of the Council was to assess the role of potassium in terms of current medical practice and future clinical applications. The primary outcome of the meeting was the development of guidelines for potassium replacement therapy. These guidelines represent a consensus of the Council members and are intended to provide a general approach to the prevention and treatment of hypokalemia.

Arrhythmias, Cardiac↗
PubMed1986

Observation of intracellular potassium and sodium in the heart by NMR: a major fraction of potassium is "invisible".

Using 39K and 23Na NMR in conjunction with extracellularly localized shift reagents, we have determined the intracellular concentrations of NMR visible sodium and potassium in isolated, perfused rat hearts. We find this concentration to be 9.9 mM/kg cell water for sodium and 31 mM/kg cell water for potassium. Values of activity determined by ion-sensitive microelectrodes are in good agreement with our sodium value but do not agree with our potassium value. Our results mean that a major pool of intracellular potassium is, on average, significantly immobilized and that the mobile NMR visible fraction (31 mM/kg) is not in exchange with the NMR invisible pool (114 mM/kg). The immobilized fraction is characterized by T2 values which are too short to be observed by our conventional spectrometer. This fraction is, therefore, said to be "invisible" under our experimental conditions.

Animals↗
PubMed1984

Lack of influence of beta adrenergic blockade on serum potassium during an infusion of potassium.

The extent to which the serum potassium rose in a group of six healthy volunteers during an intra-venous infusion of potassium was identical following pretreatment with placebo, low or high dose propranolol and low or high dose metoprolol. Thus in this acute study, we were unable to demonstrate any influence of either selective or non-selective beta adrenergic blockade upon potassium uptake mechanisms. This is in contrast to the effects of beta blockers on potassium reuptake rates noted after exercise and during cardiac surgery.

Adult↗
PubMed1994

Potassium currents in epilepsy: effects of the epileptogenic agent pentylenetetrazol on a cloned potassium channel.

The effect of the epileptogenic agent pentylenetetrazol (PTZ) on the cloned rat brain potassium channel Kv1.1 (labelled also RCK1) was investigated in the Xenopus laevis oocyte expression system. The Kv1.1 channel was affected by PTZ in a voltage-dependent manner. PTZ increased the potassium currents at more negative potentials and decreased them at more positive potentials. At a potential of -50 mV the potassium currents were increased by 0.97 and at -20 mV decreased by 0.21 of control value with 100 mmol/l PTZ. The potential at which the inversion from increase to decrease occurred was -33 mV. The inactivation characteristic of the current was shifted to more negative potentials by PTZ. The PTZ effect was obtained at a threshold concentration of 1 mmol/l and increased with rising PTZ concentrations. After removal of the tissues covering the oocyte membrane, the PTZ effect was augmented; with a concentration of 10 mmol/l PTZ the potassium currents at 0 mV were decreased by 0.04 in oocytes with covering tissues and by 0.27 of control value in oocytes without covering tissues. Under current-clamp conditions, PTZ decreased small depolarizations and increased larger depolarizations. This effect of PTZ represents a 'discriminatory function' that may contribute to epileptogenesis in nervous tissues.

Animals↗
PubMed1991

Measurements of the extracellular potassium concentrations in the isolated rabbit retina with different kinds of potassium-sensitive microelectrodes.

When the dark-adapted isolated rabbit retina has been superfused from one side with a plasma-saline mixture containing 3.5 mM potassium, the extracellular potassium concentration within the dark-adapted retina was significantly higher (4.5-6.1 mM) than the potassium of the superfusate, when measured with an electrode filled with Corning 477317. The substantial difference between the [K+]0 of the perfusate and the [K+]0 within the retina is difficult to explain and could be an instrumental artefact. To probe this possibility measurements have now been repeated using 2 different K+ electrodes, one filled with Corning 477317 and the other filled with a valinomycin-based ion exchanger. With the latter electrodes there was practically no gradient between the [K+]0 in the retina (3.2-4.0 mM) and the potassium concentration of the superfusate. It is thus evident that the earlier enigmatic values for [K+]0 relate to the use of Corning 477317-filled K+ electrodes. When, however, changes in [K+]0 were induced by a light stimulus, the measured magnitudes of change in [K+]0 were the same with the 2 types of electrode.

Animals↗
PubMed1991

In vitro loss of potassium from erythrocytes during the 0-108 h postmortem period in rats: relationship between potassium loss and postmortem interval.

A simple technique was employed for measurement of potassium loss (K(los)s) from normal and from postmortem rat erythrocytes during controlled exposure to physiologically isosmotic NaCl solution. Potassium loss from the cells decreased in a (non-linear) time-related manner during the 0-108 h postmortem period; expression of the data in the form of a double logarithmic plot (log K(loss) versus log postmortem interval (PMI) linearized the relationship between 18 and 108 h post mortem (r = -0.86; P less than 0.001 (n = 24)). Experimental data revealed that the observed postmortem changes in K(loss) were associated with and probably resulted from, the postmortem decrease in magnitude of the potassium concentration gradient across the erythrocyte membrane. Attention is drawn to the possibility of utilizing measurements of in vitro loss of potassium from erythrocytes as a means of estimating time elapsed since death.

Animals↗
PubMed1985

Is the potassium channel distribution in glial cells optimal for spatial buffering of potassium?

Glial cells in the nervous system are believed to reduce changes of extracellular potassium concentration ([K+]o), caused by neural activity, by carrying out spatial buffering of potassium. In the case of retinal glial cells (Müller cells), light-evoked increases of [K+]o within the retina are reduced by K ions flowing through the Müller cell to the vitreous fluid of the eye. We have calculated the optimal way to distribute the potassium conductance of the Müller cell to maximize spatial buffering to the vitreous fluid. The best distribution is with half the potassium conductance in the outer part of the cell, where K+ enters, and half the conductance in the vitreal endfoot, where K+ leaves the cell. This calculated distribution is very different from the actual distribution measured by Newman (1984, Nature [Lond.], 309: 155-157), where only 6% of the Müller cell conductance is in the outer cell and 94% is in the endfoot. The experimentally observed distribution gives less than a quarter of the spatial buffering that would be produced by the optimal distribution. The possible advantages of this arrangement are discussed.

Animals↗
PubMed1987

Intra- and extracellular potassium activities and the potassium equilibrium potential in partially depolarized human atrial cells.

Under tissue bath conditions, isolated specimens of human right atrium are characterized by the presence of large numbers of partially depolarized cells. The basis for the depolarization is still not understood. To determine if reduced intracellular potassium activity (aKi) is responsible for the low levels of maximum diastolic potential (MDP), aKi was directly measured with potassium ion-selective micro-electrodes (KISE). The effects of varying bath potassium concentration ([K+]0) on aiK and on the relationship between MDP and the potassium equilibrium potential (EK) also were determined. In 4 mM [K+]0, all specimens studied were partially depolarized (MDP = -43.9 +/- 1.3 mV [mean +/- S.E.]) and beat spontaneously. aKi was 98.1 +/- 1.5 mM, and EK was -93.3 +/- 0.4 mV. Changes in [K+]0 between 2.5 and 40 mM did not change aKi significantly. MDP was relatively insensitive to [K+]0 and was always far positive to EK over the entire range of [K+]0 studied. The ability of the KISE to reliably measure aKi in the face of the spontaneous diastolic depolarization was assessed by using acetylcholine or cooling to depress automaticity. These measures did not significantly alter the calculated aKi. The results indicate that: aKi in human atrial specimens is similar to that in atria from other mammalian species, and the low level of MDP exhibited by human atrial cells subject to conventional tissue bath conditions does not primarily result from low levels of aKi.

Body Fluids↗
PubMed2003

Characterization of sulfur speciation in low molecular weight subunits of glutenin after reoxidation with potassium iodate and potassium bromate at different pH values using x-ray absorption near-edge structure (XANES) spectroscopy.

Sulfur speciation in low molecular weight (LMW) subunits of glutenin after reoxidation with potassium iodate and potassium bromate at different pH values, aged subunits of glutenin as well as gluten, and gliadin have been investigated in situ by S K-edge X-ray absorption near-edge structure (XANES) spectroscopy. XANES spectra were analyzed quantitatively using a least-squares fitting routine to provide relative percentage contribution of different sulfur species occurring in the samples. Using potassium iodate and potassium bromate for reoxidation of reduced LMW subunits of glutenin led not only to disulfide states but also to higher oxidation states (sulfoxide state, sulfonic acid state). Strongest oxidation occurred at low pH values. Higher oxidation states were also predominantly detected in the aged subunits of glutenin, whereas the disulfide state was the main sulfur species in gluten and gliadin samples. The results showed that the oxidation state of sulfur prior to oxidation (thiol, disulfide) strongly influences sulfur speciation after oxidation. The choice of the oxidizing reagent seems to be of minor importance.

Bromates↗
PubMed1984

Oral potassium chloride and amiloride in hydrochlorothiazide-induced potassium loss.

To compare the effect of amiloride with that of oral potassium chloride (KCl) in hypokalemia, metabolic balance studies were carried out in hospitalized subjects with mild hypertension without edema who developed negative potassium balance after 4 days on hydrochlorothiazide (HCTZ). Subjects' diets contained measured amounts of sodium and potassium. While HCTZ treatment continued, oral preparations of either KCl solution or amiloride was added for 5 additional days. Potassium balance in the KCl-treated group further decreased by -44.9 +/- 32.3 mEq K+, while subjects on amiloride went into positive balance that averaged +51.7 +/- 24.1 mEq K+. Hypokalemia after HCTZ did not respond to KCl, while K+ levels rose from 3.32 +/- 0.22 to 3.67 +/- 0.26 mEq/l after amiloride.

Administration, Oral↗
PubMed1981

The regulation of potassium fluxes for the adjustment and maintenance of potassium levels in Escherichia coli.

The regulation of K+ fluxes has been studied in Escherichia coli after depletion of K+ by an osmotic shock or at steady state of potassium accumulation. In the absence of a carbon source, bacteria accumulate K+ to an intracellular level near 0.1 M about half of actively metabolizing cells. During uptake the rate of net unidirectional influx decreased with time down to zero as a plateau was reached and no efflux was observed. Accumulated K+ was not exchanged with external K+ under these conditions. In the presence of a carbon source bacteria took up potassium to an intracellular concentration near 0.2 M. Efflux was delayed: it started only when 50% of final cellular K+ has been taken up. At steady state cellular K+ was exchangeable with external K+. The removal of the carbon source or the addition of respiratory inhibitors immediately stopped the K+ influx but did not affect efflux until the cellular K+ concentration has dropped to a level near 0.1 M; residual potassium was no longer exchangeable with external potassium. Maintaining such an impermeability to K+ ion does not require energy (delta psi or ATP), even though residual K+ is concentrated 100-fold compared to K+ in the medium. These results suggest that K+ efflux is dependent on active metabolism and on the concentration of intracellular K+ above a threshold. Unidirectional influx is also regulated by intracellular K+ according to a different concentration dependence. It appears that the trkA system, which is the only functional system under these experimental conditions is not a 'pump and leak' type of transport system.

Biological Transport↗
PubMed1976

Extracellular potassium accumulation and inward-going potassium rectification in voltage clamped ventricular muscle.

Measurements of afterpotential, action potential duration, and output of a potassium-sensitive microelectrode indicate that the application of long clamp pulses (1 to 8 seconds) to frog ventricular muscle is accompanied by a change in the extracellular potassium concentration. The plot of the magnitude of the potassium accumulation against the clamped membrane potential yields an N-shaped relation similar to the "steady state" current-voltage relation. The accumulation studies confirm a strong inward-going (anomalous) potassium rectification.

Action Potentials↗
PubMed1970

Potassium ion specific electrode with high selectivity for potassium over sodium.

A new potassium electrode, made from valinomycin, which uses commercially available electrode configurations, responds to potassium ion concentrations from 1 mole per liter to below 10(-6) mole per liter. It is highly selective for potassium ion over sodium ion and divalent ions and can be used for the direct determination of potassium ion in human serumn. No significant complexing of potassiium appears to occur in normal seruin.

Anti-Bacterial Agents↗
PubMed1976

Effect of potassium-sparing diuretics on the renin-angiotensin-aldosterone system and potassium retention in heart failure.

The renin-angiotensin-aldosterone system and electrolyte levels in 11 patients with heart failure controlled on digoxin and frusemide were investigated after separate periods of Slow K, spironolactone, and amiloride therapy. When spironolactone or amiloride replaced Slow K, distinct parallel increments in the levels of renin, angiotensin II, and aldosterone resulted. Though plasma potassium was generally higher after spironolactone and amiloride than after Slow K, exchangeable potassium was similar with the three regimens. There was no significant relation between plasma potassium and concurrent exchangeable potassium.

Adult↗
PubMed1984

The effect of acute alcohol withdrawal on the serum potassium and total body potassium in heavy drinkers.

In a group of 20 patients with heavy alcohol intake a relation was found between withdrawal symptoms and fall in serum potassium. Total body potassium (TBK) was measured in all subjects and was lower in the group of subjects who displayed symptoms than in the group who did not. The subgroup of the four most severe reactors had a mean TBK value significantly less than the 'non-reactor' group. The minimum serum potassium levels observed for all subjects in the four day period following alcohol withdrawal correlated with their TBK values. We suggest that the mechanism for the serum potassium fall might be overactivity of the Na-K pump caused by ethanol consumption. There was also an association between withdrawal reaction and abnormal liver function and a transient rise in serum phosphate in the more severely reacting subjects.

Adenosine Triphosphatases↗
PubMed2000

[Potassium and arterial hypertension--are potassium supplements helpful?].

The blood pressure lowering effects of potassium are well known. Accordingly it is not surprising, that potassium supplements have been recommended as a therapeutical strategy to lower blood pressure. In this review the epidemiological data and potential physiological mechanisms of the potassium-induced cardiovascular effects will be summarized. In addition the recommendations regarding potassium intake and supplementation in hypertensive patients will be discussed.

Administration, Oral↗
PubMed1975

Active potassium transport coupled to active sodium transport in vesicles reconstituted from purified sodium and potassium ion-activated adenosine triphosphatase from the rectal gland of Squalus acanthias.

Vesicles containing a purified shark rectal gland (sodium + potassium)-activated adenosine triphosphatase-(NaK ATPase) were prepared by dialyzing for 2 days egg lecithin, cholate, and the NaK ATPase purified from the rectal gland of Squalus acanthias. These vesicles were capable of both Na+ and K+ transport. Studies of K+ transport were made by measuring the ATP-stimulated transport outward of 42K+ or 86Rb+. Vesicles were preloaded with isotope by equilibration at 4 degrees for 1 to 3 days. Transport of 42K+ or 86Rb+ was initiated by addition of MgATP to the vesicles. The ATP-dependent exit of either isotope was the same. Experiments are presented which show that this loss of isotope was not due to changes in ion binding but rather due to a loss in the amount of ion trapped in the vesicular volume. The transport of K+ was dependent on external Mg2+. CTP was almost as effective as ATP in stimulating K+ transport, while UTP was relatively ineffective. These effects of nucleotides parallel their effects on Na+ accumulation and their effectiveness as substrates for the enzyme. Potassium transport was inhibited by ouabain and required the presence of Na+. The following asymmetries were seen: (a) addition of external Mg2+ supported K+ transport; (b) ouabain inhibited K+ transport only if it was present inside the vesicles; (c) addition of external Na+ to the vesicles stimulated K+ transport. External Li+ was ineffective as a Na+ substitute. The specific requirement of external Na+ for K+ transport indicates that K+ exit is coupled to Na+ entry. Changes in the internal vesicular ion concentrations were studied with vesicles prepared in 20 mM NaCl and 50 mM KCl. After 1 hour of transport at 25 degrees, a typical Na+ concentration in the vesicles in the presence of ATP was 72 mM. A typical K+ concentration in the vesicles was 10 mM as measured with 42K+ or 6 mM as measured with 86Rb+. The following relationships have been calculated for Na+ transport, K+ transport and ATP hydrolysis: Na+/ATP = 1.42, K+/ATP =1.04, and Na+/K+ = 1.43. The ratio of 2.8 Na+ transported in to 2 K+ transported out is very close to the value reported for the red cell membrane. Potassium-potassium exchange similar to that observed in the red cell membrane and attributed to the Na+-K+ pump (stimulated by ATP and orthophosphate and inhibited by ouabain) was observed when vesicles were prepared in the absence of Na+. The results reported in this paper prove that the shark rectal gland NaK ATPase, which is 90 to 95% pure, is the isolated pump for the coupled transports of Na+ and K+.

Adenosine Triphosphatases↗