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PubMed1993

Lack of voltage sensitive potassium channels and generation of membrane potential by sodium potassium ATPase in murine T lymphocytes.

Voltage sensitive K+ channels, which are responsible for generation of membrane potential in most cells, are functionally absent in about one-third of peripheral murine T cells and greatly reduced in the rest as shown by resistance of their membrane potential to changes in extracellular potassium concentration and failure of K+ channel dependent volume regulation. Despite the absence of voltage- sensitive K+ channels, the membrane potential of peripheral T cells is between -60 and -70 mV, the same as thymocytes. A total of 40 to 70 mV of the membrane potential of peripheral T cells is produced by the direct electrogenic action of the asymmetric Na+K+ ATPase pump because the cells are depolarized by ouabain, an inhibitor of the pump, removal of extracellular potassium or reduction of temperature. The residual, ouabain-resistant membrane potential, is sensitive to the K+ channel blocker, quinine, and thus due to electrodiffusion through K+ channels. Na+ and K+ turnover, and sensitivity to ouabain, are the same in peripheral T cells and thymocytes. The predominant mechanism of membrane potential generation changes during T lymphocyte differentiation from electrodiffusion in the thymus to electrogenic in peripheral T cells and back to electrodiffusion upon peripheral cell activation.

Animals↗
PubMed2006

Vibrational spectroscopy at high pressure of the permanganate anion trapped in potassium bromide and potassium perchlorate matrices.

The effect of high pressure on the resonance Raman spectra of the permanganate ion isolated in potassium bromide and potassium perchlorate matrices has been investigated at room temperature for pressures up to 50 kbar. The pressure dependences of the anharmonicity constants and harmonic frequencies have been determined from the overtones of the totally symmetric nu1(A1) mode of the permanganate ion. For both matrices, as the pressure increases, the anharmonicity constants decrease slightly, while the harmonic frequencies increase steadily. The effect of the potassium bromide phase transition from a face-centered to a body-centered structure was observed on the permanganate ion Raman spectrum at approximately 24 kbar. The perchlorate matrix does not exhibit any phase transition under the experimental conditions used in this study.

Journal Article↗
PubMed2004

Potassium and potassium clouds in endothelium-dependent hyperpolarizations.

A small increase in extracellular K(+) acts as a local, physiological regulator of blood flow to certain vascular beds. The K(+) derives from active tissues such as contracting skeletal muscle and brain and increases blood supply to these organs by the activation of Na(+)/K(+)-ATPases and/or inwardly-rectifying K(+) channels on the vascular myocytes. K(+) liberated from the vascular endothelium also acts as an endothelium-derived hyperpolarizing and relaxing factor within blood vessels. The K(+) effluxes from endothelial cell intermediate- and small-conductance, Ca(2+)-sensitive K(+) channels which open in response to stretch and local hormones. In many vessels, endothelium-derived hyperpolarizing factor (EDHF) seems identical to the K(+) derived from endothelial cells; it activates Na(+)/K(+)-ATPases (particularly those containing alpha2 and alpha3 subunits) and inward rectifiers (particularly Kir2.1) located on the vascular myocytes. Vasospastic agents generate "potassium clouds" around vascular smooth muscle cells via the efflux of this ion through large conductance, Ca(2+)-sensitive K(+) channels on the myocytes. These potassium clouds can reduce the hyperpolarizing actions of endothelium-derived K(+) by effectively saturating the Na(+)/K(+)-ATPases and inward rectifiers on the muscle cells and they may be of clinical significance in vasospastic conditions.

Animals↗
PubMed1977

Sodium and potassium intakes and excretions of normal men consuming sodium chloride or a 1:1 mixture of sodium and potassium chlorides.

Two groups of 10 healthy young men were matched on the basis of their free-choice consumptions of regular table salt. For 28 days they were then fed carefully controlled low-sodium foods. One group was permitted free-choice seasoning of these foods with regular table salt, the other with a 1:1 mixture of sodium and potassium chlorides. Intakes and urinary and fecal excretions of sodium and potassium were determined by analysis. The results were: 1) the subjects salted their food with essentially the same amounts of regular table salt as of the 1:1 mixture; 2) the sodium intake associated with seasoning at the table was reduced with the 1:1 mixture to 44 percent of the amount consumed with regular table salt; and 3) over a 28-day period there was no tendency for subjects to increase their use of a 1:1 mixture, when used in place of regular table salt, to compensate for their reduced sodium intakes. Under the conditions of this study, the use of the 1:1 mixture as a seasoning agent for foods that contained no added salt resulted in an average total intake of sodium (food plus seasoning) which was 55 percent that of the subjects using regular table salt.

Adult↗
PubMed1993

Inhibitory effect of potassium citrate on rat renal tumors induced by N-ethyl-N-hydroxyethylnitrosamine followed by potassium dibasic phosphate.

Potassium dibasic phosphate (PDP) was administered at a concentration of 10% by weight in basal diet to unilaterally nephrectomized Wistar rats previously given 1000 ppm N-ethyl-N-hydroxyethyl-nitrosamine (EHEN) in the diet for 2 weeks. To study the effect of alkalinization on renal mineralization, some animals concomitantly received 5% potassium citrate (PC). Feeding PDP alone promoted adenomatous hyperplasias, which were regarded as preneoplastic lesions, as well as renal cell tumors in EHEN-initiated rats, whereas the addition of PC to PDP diets reduced the promoting effect. Histopathology, serum biochemistry and urinalysis indicated retardation of renal calcium crystallization by PC. Two other phosphate salts, sodium phosphate (SP) and calcium phosphate (CP), were also administered. SP showed a slight promoting effect on adenomatous hyperplasias and a 2-fold increase in the yield of renal cell tumors, while CP induced a clear reduction of both lesions, over EHEN alone. The promoting effects of both PDP and SP and the inhibitory effect of PC were somewhat correlated to 5-bromo-2'-deoxyuridine labeling indices, the degree of nephropathy, and mineralization in the kidney. Immunohistochemically, the nephropathy induced by phosphate salts was not linked to alpha 2u-globulin. A pathogenesis for renal carcinogenesis is suggested in which nephropathy associated with mineralization enhances the development of renal cell tumors.

Alpha-Globulins↗
PubMed2000

Potassium inhibition of sodium-activated potassium (K(Na)) channels in guinea-pig ventricular myocytes.

N(a+)-activated potassium channels (K(Na) channels) were studied in inside-out patches from guinea-pig ventricular myocytes at potentials between -100 and +80 mV. External K(+) (K(+)(o)) was set to 140 mM. For inwardly directed currents with 105 mM internal K(+) (K(+)(1)), the unitary current-voltage relationship was fitted by the constant field equation with a potassium permeability coefficient, P(K), of 3.72 x 10(-13) cm(3) s(-1). The slope conductance (-100 to -10 mV) was 194 +/- 4.5 pS (mean +/- s.d., n = 4) with 105 mM K(+)(i) (35 mM Na(+)(i)) but it decreased to 181 +/- 5.6 pS (n = 5) in 70 mM K(+)(i) (70 mM Na(+)(i)). K(Na) channels were activated by internal Na(+) in a concentration-dependent fashion. With 4 mM K(+)(i), maximal activation was recorded with 100 mM Na(+)(i) (open probability, P(o), about 0.78); half-maximal activation required about 35 mM Na(+)(i). When K(+)(i) was increased to 70 mM, half-maximal activation shifted to about 70 mM Na(+)(i). With Na(+)(i) set to 105 mM, channel activity was markedly inhibited when K(+)(i) was increased from 35 to 105 mM. Channel openings were abolished with 210 mM K(+)(i). The inhibitory effect of internal K(+) was also observed at more physiological conditions of osmolarity, ionic strength and chloride concentration. With 35 mM Na(+)(i) and 4 mM K(+)(i), P(o) was 0.48 +/- 0.10 (n = 6); when K(+)(i)was increased to 35 mM, P(o) was reduced to 0.04 +/- 0.05 (n = 7, P < 0.001). The relationship between P(o) and Na(+)(i) concentration at different levels of K(+)(i) is well described by a modified Michaelis-Menten equation for competitive inhibition; the Hill coefficients were 4 for the P(o)-Na(+)(i) relationship and 1.2 for the P(o)-K(+)(i) relationship. It is suggested that Na(+) and K(+) compete for a superficial site on the channel's permeation pathway. K(Na) channels would be most likely to be activated in vivo when an increase in Na(+)(i) is accompanied by a decrease of K(+)(i).

Adenosine Triphosphate↗
PubMed2004

Selective block of the human 2-P domain potassium channel, TASK-3, and the native leak potassium current, IKSO, by zinc.

Background potassium channels control the resting membrane potential of neurones and regulate their excitability. Two-pore-domain potassium (2-PK) channels have been shown to underlie a number of such neuronal background currents. Currents through human TASK-1, TASK-2 and TASK-3 channels expressed in Xenopus oocytes were inhibited by extracellular acidification. For TASK-3, mutation of histidine 98 to aspartate or alanine considerably reduced this effect of pH. Zinc was found to be a selective blocker of TASK-3 with virtually no effect on TASK-1 or TASK-2. Zinc had an IC(50) of 19.8 microM for TASK-3, at +80 mV, with little voltage dependence associated with this inhibition. TASK-3 H98A had a much reduced sensitivity to zinc suggesting this site is important for zinc block. Surprisingly, TASK-1 also has histidine in position 98 but is insensitive to zinc block. TASK-3 and TASK-1 differ at position 70 with glutamate for TASK-3 and lysine for TASK-1. TASK-3 E70K also had a much reduced sensitivity to zinc while the corresponding reverse mutation in TASK-1, K70E, induced zinc sensitivity. A TASK-3-TASK-1 concatamer channel was comparatively zinc insensitive. For TASK-3, it is concluded that positions E70 and H98 are both critical for zinc block. The native cerebellar granule neurone (CGN) leak current, IK(SO), is sensitive to block by zinc, with current reduced to 0.58 of control values in the presence of 100 microM zinc. This suggests that TASK-3 channels underlie a major component of IK(SO). It has recently been suggested that zinc is released from inhibitory synapses onto CGNs. Therefore it is possible that inhibition of IK(SO) in cerebellar granule cells by synaptically released zinc may have important physiological consequences.

Animals↗
PubMed1985

Renal adaptation to potassium in the adrenalectomized rabbit. Role of distal tubular sodium-potassium adenosine triphosphatase.

Potassium secretion and sodium-potassium adenosine triphosphatase (Na-K-ATPase) activity in the distal nephron segments are known to be influenced by the dietary intake of K+. This has been attributed to a change in the plasma aldosterone level, which also influences K+ secretion and Na-K-ATPase activity in the distal nephron. To investigate whether or not dietary K+ can modulate Na-K-ATPase activity in the distal nephron independently of aldosterone, we determined Na-K-ATPase activity in four distinct nephron segments of adrenalectomized (adx) rabbits given four specific diets for 1 wk before experimentation. Na-K-ATPase activity was determined by a fluorometric microassay in which ATP hydrolysis is coupled to NADH oxidation. The nephron segments examined were the distal convoluted tubule (DCT), the connecting tubule (CNT), the cortical collecting duct (CCD), and the outer medullary collecting duct (MCD). All diets were similar in composition except for their K+ contents, which were 100, 300, 500, and 700 meq/kg in groups 1-4, respectively. In these adx animals, Na-K-ATPase activity increased greater than 200% in the CCD as the dietary intake of K+ increased. There was a linear relationship between K+ excretion and the enzyme activity in this segment. There was a 50% increase in Na-K-ATPase activity in the CNT as the dietary intake of K+ increased in adx animals. However, there were no significant differences in Na-K-ATPase activities in the DCT and MCD among the four treatment groups. It is concluded that dietary K+ intake can influence Na-K-ATPase activity in the CCD and CNT independently of plasma aldosterone levels.

Adaptation, Physiological↗
PubMed2005

Using Healthcare Failure Mode and Effect Analysis tool to review the process of ordering and administrating potassium chloride and potassium phosphate.

During the spring of 2004, in the Calgary Health Region (CHR) two critical incidents occurred involving patients receiving continuous renal replacement therapy (CRRT) in the intensive care unit (ICU). The outcome of these events resulted in the sudden death of both patients. The Department of Critical Care Medicine's Patient Safety and Adverse Events Team (PSAT), utilized the Healthcare Failure Mode and Effect Analysis (HFMEA) tool to review the process and conditions surrounding the ordering and administration of potassium chloride (KCI) and potassium phosphate (KPO4) in our ICUs. The HFMEA tool and the multidisciplinary team structure provided a solid framework for systematic analysis and prioritization of areas for improvement regarding the use of intravenous, high-concentration KCL and KPO4 in the ICU.

Aged, 80 and over↗
PubMed2000

Potassium supplements' effect on potassium balance in athletes during prolonged hypokinetic and ambulatory conditions.

Electrolyte supplements may be used to prevent changes in electrolyte balance during hypokinesia (diminished movement). The aim of this study was to measure the effect of potassium (K) supplements on K balance 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 25.1+/-4.4 yr were chosen as subjects. They were divided equally into four groups: unsupplemented ambulatory control subjects (UACS), unsupplemented hypokinetic subjects (UHKS), supplemented hypokinetic subjects (SHKS) and supplemented ambulatory control subjects (SACS). The SHKS and UHKS groups were kept under an average walking distance of 0.7 km/d. The SACS and SHKS groups were supplemented daily with 50.0 mg elemental potassium chloride (KCl) per kilogram body weight. The K balance, fecal K excretion, urinary K, sodium (Na), and chloride (Cl) excretion, plasma K, Na, and Cl concentration, plasma renin activity (PRA) and plasma aldosterone (PA) concentration, anthropometric characteristics and peak oxygen uptake were measured. Negative K balance, fecal K excretion, urinary K, Na, and Cl excretion, plasma K, Na, and Cl concentration, and PRA and PA concentration increased significantly (p < or = 0.01), whereas body weight and peak oxygen uptake decreased significantly in the SHKS and UHKS groups when compared with SACS and UACS groups. However, the measured parameters changed much faster and much more in SHKS group than UHKS group. By contrast, K balance, fecal, urinary, and plasma K, plasma hormones, body weight, and peak oxygen uptake did not change significantly in the SACS and UACS groups when compared with the baseline control values. It was concluded that prolonged HK induces a significant negative K balance associated with increased plasma K concentration and urinary and fecal K excretion. However, negative K balance appeared much faster and was much greater in the SHKS group than UHKS group. Thus, K supplementation was not effective in preventing negative K balance during prolonged HK.

Adult↗
PubMed2003

Potassium channel blockers tetraethylammonium and 4-aminopyridine fail to prevent microglial activation induced by elevated potassium concentration.

The effect of potassium channel blocker tetraethylammonium and 4-aminopyridine was examined on the elevated K+ concentration-induced microglial activation on rat hippocampal slice preparations. Microglial cells were detected by immunohistochemisty with a monoclonal antibody (OX 42) raised against a type 3 complement receptor. During activation the morphology of the microglial cells changes and the staining intensity increases. The degree of microglial activation was determined by measuring the integrated optical density of the cells. Tetraethylammonium and 4-aminopyridine failed to reduce the elevated K+ concentration-induced microglial activation. Both potassium channel blockers, when applied on the hippocampal slices without K+, caused significantly increased microglial activation as compared to the control slices. In order to check whether the functional alteration of the neuronal population induced by 4-aminopyridine caused the activation of the microglial cells, Schaffer collaterals were cut to block spreading of epileptiform hyperactivity of the CA3 pyramidal cells to the CA1 region. No significant differences were found in microglial activation between the CA3 and CA1 regions, indicating that the effect of 4-aminopyridine on microglial cells is independent of the epileptiform activity caused by the drug.

4-Aminopyridine↗
PubMed1994

Inhibitory properties of NIP-121, a potassium channel opener, on high potassium- and norepinephrine-induced contraction and calcium mobilization in rat aorta.

We examined the effects of NIP-121, a potassium channel opener, on KCl- and norepinephrine (NE)-induced contraction, the phasic-contraction under the Ca(2+)-free condition and cytosolic free-Ca2+ mobilization using isolated rat aorta. NIP-121 as well as cromakalim inhibited, in the KCl- and NE-contractions concentration dependently. Glibenclamide, an ATP-sensitive potassium channel blocker, competitively reversed their inhibition. On the other hand, they did not inhibit the phasic-contractions induced by NE in Ca(2+)-free medium. In Fura-2-loaded rat aorta, NIP-121 inhibited only the late phase of the NE-induced cytosolic Ca2+ level ([Ca2+]cyt) increases that were inhibited by nicardipine. However, it did not inhibit the first [Ca2+]cyt increase, which was completely abolished by repeated applications of NE in Ca(2+)-free medium. Neither did it inhibit phorbol ester-induced contraction. The vasorelaxant mechanism of NIP-121 is attributable to the decrease in Ca2+ influx passing through the membrane Ca2+ permeable systems. In addition, inhibition of Ca2+ release from sarcoplasmic reticulum (SR) and of protein kinase C (PKC) activation may not be involved in vasorelaxation induced by NIP-121.

Animals↗
PubMed1983

Studies on slow cardiac action potentials occurring in potassium-rich media as a simulation of the early phase of myocardial infarction. Influence of potassium-conductance blockers and antiarrhythmic drugs.

In the acute phase of myocardial infarction, a marked intracellular potassium loss and the lack of intact coronary circulation are known to result in extracellular hyperpotassemia partially depolarizing the damaged cells. To simulate these conditions, isolated guinea pig papillary muscles were superfused with K+-rich Tyrode solution, the minimal norepinephrine concentration required to trigger slow action potentials (SR) was measured, and the characteristics of SR were studied with glass microelectrodes. The threshold norepinephrine concentration was found to be about 1.04 x 10(-6)M. This threshold concentration was decreased by substances inhibiting the outward potassium currents (4-aminopyridine, tetraethylammonium, cesium); the SR duration and the maximal rate of depolarization were increased by them. Lidocaine and procainamide have no influence on these parameters. Phenytoin and the Mg2+ ion were found to have a marked inhibitor effect by increasing the threshold norepinephrine concentration and decreasing the maximal rate of depolarization of SR.

Action Potentials↗
PubMed1986

Single-channel analysis of the potassium permeability in HeLa cancer cells: evidence for a calcium-activated potassium channel of small unitary conductance.

Cell-attached and inside-out patch-clamp experiments (O.P. Hamill et al., Pfluegers Arch. 391:85-100, 1981) were undertaken in order to characterize the molecular mechanisms responsible for the calcium-dependent potassium permeability observed in HeLa cancer cells. Our result essentially indicate that the HeLa cell external membrane contains potassium channels whose activity can be triggered within an internal calcium concentration range of 0.1 to 1 microM. This particular channel was found to behave as an inward rectifier in symmetrical 200 mM KCl with a conductance of 50 and 10 pS at large negative and large positive membrane potentials, respectively. I/V curves were also measured in 10, 20, 75, 200 and 300 mM KCl and the data interpreted in terms of a one-site-two-barrier model. The channel activity appeared to be nearly voltage independent within the voltage range -100 to +100 mV, an increase of Po, the open channel probability, being observed at large negative potentials only. In addition, the results obtained from inside-out experiments on the relationship between Po and the cytoplasmic free-calcium concentration have led to conclude that four calcium ions are probably required in order to open the channel. In this regard it was found that an increase of the internal free-calcium level affects more the number of channel openings per second than the actual channel mean lifetime. Finally, it is concluded following a time interval distribution analysis, that this particular channel has at least three closed states and two open states.

Calcium↗
PubMed1991

Low potassium-type but not high potassium-type sheep red blood cells show passive K+ transport induced by low ionic strength.

Low potassium-type (LK) sheep red blood cells show a significant increase of the residual (i.e., ouabain-insensitive) K+ influx when the ionic strength of the solution is decreased. This effect is absent from high potassium-type (HK) sheep red blood cells. The KCl cotransport system is not involved since three different manoeuvres to suppress the KCl cotransport (replacement of Cl- by NO3-, volume-decrease, inhibition by anti-L1 antibodies) have no effect on the low ionic strength-stimulated K+ influx.

Animals↗
PubMed1994

Zinc ions block rectifier potassium channels and calcium activated potassium channels at the frog motor nerve endings.

The effect of Zn2+ on presynaptic currents was investigated on frog cutaneous pectoris nerve-muscle preparations. Nerve terminal spikes were recorded with extracellular electrodes placed in the perineurial sheaths of motor nerves. Zinc ions reversibly suppressed the component of the waveform associated with K+ currents--unmasking an inward current at the terminal--and induced repetitive firing when were applied to preparations perfused with calcium containing solutions. In experiments in which delayed rectifier channels were blocked by 3,4-diaminopyridine, Zn2+ caused a prolonged and reversible inward current associated with a slight decrease in the peak calcium current generated by 3,4-diaminopyridine. Zinc ions abolished the plateau calcium current produced by the simultaneous action of 3,4-diaminopyridine and tetraethylammonium. Finally, in all the preparations in which the exposure to Zn2+ was prolonged it was observed a dramatic and irreversible reduction of the presynaptic currents. These results suggest that Zn2+ has, at least, four different effects on presynaptic currents: (1) blockade of delayed rectifier potassium currents, (2) blockade of calcium-activated potassium currents, (3) blockade of calcium currents and (4) a delayed and irreversible disruption of all ionic conductances of the terminal.

4-Aminopyridine↗
PubMedDate not supplied

Induction of micronucleated reticulocytes by potassium bromate and potassium chromate in CD-1 male mice.

Micronucleus tests of potassium bromate (KBrO3) and potassium chromate (K2CrO4) were conducted with peripheral blood reticulocytes (PB-RETs) of CD-1 male mice dose intraperitoneally. Peripheral blood cells collected from the tail were stained supravitally with acridine orange (AO) using AO-coated glass slides. Both KBrO3 and K2CrO4 induced micronuclei in PB-RETs in the same manner as in polychromatic erythrocytes of bone marrow.

Animals↗
PubMed1993

Halothane acts on many potassium channels, including a minimal potassium channel.

There has been considerable controversy over whether general anesthetics act directly on membrane proteins, and if so, whether there are uniquely sensitive protein targets upon which they act. Here, we examine the actions of halothane on a diverse collection of voltage-gated potassium channels expressed in Xenopus oocytes, and find that they are all sensitive at clinically relevant concentrations. To investigate further the molecular basis of this commonality, human and rat minimal potassium (minK) channels, which have exceedingly short amino acid sequences, were examined. Current through these channels is reversibly reduced to 68% of control values by 0.5% (0.34 mM) halothane. A double deletion mutant of the 130-amino acid minK protein, in which 30 amino acids of the N-terminus, thought to be extracellular, and 37 amino acids of the putative intracellular C-terminus are deleted (resulting in a protein in which more than half of both the extracellular and intracellular domains have been removed) responds to low halothane concentrations similarly to the parent channel. While alternative explanations are possible, this result is consistent with a model whereby halothane interacts with the channel protein from within the lipid bilayer.

Animals↗