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K+ Concentration (k+ + concentration)
Kinds of K+ Concentration Selected AbstractsInfluence of Extracellular K+ Concentrations on Quinidine-induced K+ Current Inhibition in Rat Ventricular MyocytesJOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 1 2000MICHIKO HIROTA Hypokalaemia is one of the important risk factors for development of torsades de pointes. We recently reported that hypokalaemia increased the electrocardiographic QT interval in rats treated with quinidine, but did not alter the arrhythmogenic potency of quinidine. In this study, we have investigated the influence of extracellular potassium concentration ([K+]o) on the inhibition of several types of cardiac potassium currents by quinidine. Such types of currents include the delayed rectifier potassium current (IK), the transient outward current (Ito), and the inward rectifier potassium current (IK1), as measured in isolated rat ventricular cells using patch-clamp techniques. Concentration-dependent effects of quinidine on IK, Ito, and IK1 were evaluated under both normal ([K+]o = 5.4 mM) and hypokalaemic ([K+]o = 3.5 mM) conditions. In contrast to both IK and Ito, which were barely influenced by changes in [K+]o, IK1 was significantly inhibited by hypokalaemia. Furthermore, while quinidine suppressed both IK and Ito in a concentration-dependent manner, the inhibitory potency of quinidine on these currents was not influenced by changes in [K+]o. The respective normal and hypokalaemic IC50 values for quinidine were 11.4 and 10.0 ,M (IK), and 17.6 and 17.3 ,M (Ito). Although higher concentrations of quinidine were required to inhibit IK1, the inhibitory potency of quinidine was also found to be insensitive to changes in [K+]o. Thus, in rats, the inhibitory potency of quinidine for the K+ current-types IK, Ito and IK1 is barely influenced by changes in [K+]o. These findings are consistent with our previous report showing that the QT-prolonging potency of quinidine was not altered under hypokalaemic conditions. However, whilst hypokalaemia does not affect IK or Ito, it can inhibit IK1 and can result in QT prolongation in-vivo. [source] Potassium-transporting proteins in skeletal muscle: cellular location and fibre-type differencesACTA PHYSIOLOGICA, Issue 2 2010M. Kristensen Abstract Potassium (K+) displacement in skeletal muscle may be an important factor in the development of muscle fatigue during intense exercise. It has been shown in vitro that an increase in the extracellular K+ concentration ([K+]e) to values higher than approx. 10 mm significantly reduce force development in unfatigued skeletal muscle. Several in vivo studies have shown that [K+]e increases progressively with increasing work intensity, reaching values higher than 10 mm. This increase in [K+]e is expected to be even higher in the transverse (T)-tubules than the concentration reached in the interstitium. Besides the voltage-sensitive K+ (Kv) channels that generate the action potential (AP) it is suggested that the big-conductance Ca2+ -dependent K+ (KCa1.1) channel contributes significantly to the K+ release into the T-tubules. Also the ATP-dependent K+ (KATP) channel participates, but is suggested primarily to participate in K+ release to the interstitium. Because there is restricted diffusion of K+ to the interstitium, K+ released to the T-tubules during AP propagation will be removed primarily by reuptake mediated by transport proteins located in the T-tubule membrane. The most important protein that mediates K+ reuptake in the T-tubules is the Na+,K+ -ATPase ,2 dimers, but a significant contribution of the strong inward rectifier K+ (Kir2.1) channel is also suggested. The Na+, K+, 2Cl, 1 (NKCC1) cotransporter also participates in K+ reuptake but probably mainly from the interstitium. The relative content of the different K+ -transporting proteins differs in oxidative and glycolytic muscles, and might explain the different [K+]e tolerance observed. [source] Effects of Potassium Concentration on Firing Patterns of Low-Calcium Epileptiform Activity in Anesthetized Rat Hippocampus: Inducing of Persistent Spike ActivityEPILEPSIA, Issue 4 2006Zhouyan Feng Summary:,Purpose: It has been shown that a low-calcium high-potassium solution can generate ictal-like epileptiform activity in vitro and in vivo. Moreover, during status epileptiform activity, the concentration of [K+]o increases, and the concentration of [Ca2+]o decreases in brain tissue. Therefore we tested the hypothesis that long-lasting persistent spike activity, similar to one of the patterns of status epilepticus, could be generated by a high-potassium, low-calcium solution in the hippocampus in vivo. Methods: Artificial cerebrospinal fluid was perfused over the surface of the exposed left dorsal hippocampus of anesthetized rats. A stimulating electrode and a recording probe were placed in the CA1 region. Results: By elevating K+ concentration from 6 to 12 mM in the perfusate solution, the typical firing pattern of low-calcium ictal bursts was transformed into persistent spike activity in the CA1 region with synaptic transmission being suppressed by calcium chelator EGTA. The activity was characterized by double spikes repeated at a frequency ,4 Hz that could last for >1 h. The analysis of multiple unit activity showed that both elevating [K+]o and lowering [Ca2+]o decreased the inhibition period after the response of paired-pulse stimulation, indicating a suppression of the after-hyperpolarization (AHP) activity. Conclusions: These results suggest that persistent status epilepticus,like spike activity can be induced by nonsynaptic mechanisms when synaptic transmission is blocked. The unique double-spike pattern of this activity is presumably caused by higher K+ concentration augmenting the frequency of typical low-calcium nonsynaptic burst activity. [source] Electrical and Chemical Long-term Depression Do Not Attenuate Low-Mg2+,induced Epileptiform Activity in the Entorhinal CortexEPILEPSIA, Issue 4 2005Jörg Solger Summary:,Purpose: Low-frequency electrical and magnetic stimulation of cortical brain regions has been shown to reduce cortical excitability and to decrease the susceptibility to seizures in humans and in vivo models of epilepsy. The induction of long-term depression (LTD) or depotentiation of a seizure-related long-term potentiation has been proposed to be part of the underlying mechanism. With the low-Mg2+ -model of epilepsy, this study investigated the effect of electrical LTD, chemical LTD, and depotentiation on the susceptibility of the entorhinal cortex to epileptiform activity. Methods: The experiments were performed on isolated entorhinal cortex slices obtained from adult Wistar rats and mice. With extracellular recording techniques, we studied whether LTD induced by (a) three episodes of low-frequency paired-pulse stimulation (3 × 900 paired pulses at 1 Hz), and by (b) bath-applied N -methyl- d -aspartate (NMDA, 20 ,M) changes time-to-onset, duration, and frequency of seizure-like events (SLEs) induced by omitting MgSO4 from the artificial cerebrospinal fluid. Next we investigated the consequences of depotentiation on SLEs themselves by applying low-frequency stimulation after onset of low-Mg2+,induced epileptiform activity. Results: LTD, induced either by low-frequency stimulation or by bath-applied NMDA, had no effect on time-to-onset, duration, and frequency of SLEs compared with unconditioned slices. Low-frequency stimulation after onset of SLEs did not suppress but induced SLEs that lasted for the time of stimulation and were associated with a simultaneous increase of the extracellular K+ concentration. Conclusions: Our study demonstrates that neither conditioning LTD nor brief low-frequency stimulation decreases the susceptibility of the entorhinal cortex to low-Mg2+,induced epileptiform activity. The present study does not support the hypothesis that low-frequency brain stimulation exerts its anticonvulsant effect via the induction of LTD or depotentiation. [source] Synaptic and non-synaptic mechanisms of amygdala recruitment into temporolimbic epileptiform activitiesEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 10 2003Julia Klueva Abstract Lateral amygdala (LA) activity during synchronized-epileptiform discharges in temporolimbic circuits was investigated in rat horizontal slices containing the amygdala, hippocampus (Hip), perirhinal (Prh) and lateral entorhinal (LEnt) cortex, through multiple-site extra- and intracellular recording techniques and measurement of the extracellular K+ concentration. Application of 4-aminopyridine (50 µm) induced epileptiform discharges in all regions under study. Slow interictal-like burst discharges persisted in the Prh/LEnt/LA after disconnection of the Hip, seemed to originate in the Prh as shown from time delay analyses, and often preceded the onset of ictal-like activity. Disconnection of the amygdala resulted in de-synchronization of epileptiform discharges in the LA from those in the Prh/LEnt. Interictal-like activity was intracellularly reflected in LA projection neurons as ,-aminobutyric acid (GABA)A/B receptor-mediated synaptic responses, and depolarizing electrogenic events (spikelets) residing on the initial phase of the GABA response. Spikelets were considered antidromically conducted ectopic action potentials generated at axon terminals, as they were graded in amplitude, were not abolished through hyperpolarizing membrane responses (which effectively blocked evoked orthodromic action potentials), lacked a clear prepotential or synaptic potential, were not affected through blockers of gap junctions, and were blocked through remote application of tetrodotoxin at putative target areas of LA projection neurons. Remote application of a GABAB receptor antagonist facilitated spikelet generation. A transient elevation in the extracellular K+ level averaging 3 mm above baseline occurred in conjunction with interictal-like activity in all areas under study. We conclude that interictal-like discharges in the LA/LEnt/Prh spread in a predictable manner through the synaptic network with the Prh playing a leading role. The rise in extracellular K+ may provide a depolarizing mechanism for recruitment of interneurons and generation of ectopic action potentials at axon terminals of LA projection neurons. Antidromically conducted ectopic action potentials may provide a spreading mechanism of seizure activity mediated by diffuse axonal projections of LA neurons. [source] Potassium channel Kir4.1 macromolecular complex in retinal glial cellsGLIA, Issue 2 2006Nathan C. Connors Abstract A major role for Müller cells in the retina is to buffer changes in the extracellular K+ concentration ([K+]o) resulting from light-evoked neuronal activity. The primary K+ conductance in Müller cells is the inwardly rectifying K+ channel Kir4.1. Since this channel is constitutively active, K+ can enter or exit Müller cells depending on the state of the [K+]o. This process of [K+]o buffering by Müller cells ("K+ siphoning") is enhanced by the precise accumulation of these K+ channels at discrete subdomains of Müller cell membranes. Specifically, Kir4.1 is localized to the perivascular processes of Müller cells in animals with vascular retinas and to the endfeet of Müller cells in all species examined. The water channel aquaporin-4 (AQP4) also appears to be important for [K+]o buffering and is expressed in Müller cells in a very similar subcellular distribution pattern to that of Kir4.1. To gain a better understanding of how Müller cells selectively target K+ and water channels to discrete membrane subdomains, we addressed the question of whether Kir4.1 and AQP4 associate with the dystrophin,glycoprotein complex (DGC) in the mammalian retina. Immunoprecipitation (IP) experiments were utilized to show that Kir4.1 and AQP4 are associated with DGC proteins in rat retina. Furthermore, AQP4 was also shown to co-precipitate with Kir4.1, suggesting that both channels are tethered together by the DGC in Müller cells. This work further defines a subcellular localization mechanism in Müller cells that facilitates [K+]o buffering in the retina. © 2005 Wiley-Liss, Inc. [source] Few cultured rat primary sensory neurons express a tolbutamide-sensitive K+ currentJOURNAL OF CELLULAR AND MOLECULAR MEDICINE, Issue 2 2002Violeta Ristoiu Abstract The response of dorsal root ganglion (DRG) neurons to metabolic inhibition is known to involve calcium-activated K+ channels; in most neuronal types ATP-sensitive K+ channels (KATP) also contribute, but this is not yet established in the DRG. We have investigated the presence of a KATP current using whole-cell recordings from rat DRG neurons, classifying the neurons functionally by their "current signature" (Petruska et al, J Neurophysiol 84: 2365,2379, 2000). We clearly identified a KATP current in only 1 out of 62 neurons, probably a nociceptor. The current was activated by cyanide (2 mM NaCN) and was sensitive to 100 ,M tolbutamide; the relation between reversal potential and external K+ concentration indicated it was a K+ current. In a further two neurons, cyanide activated a K+ current that was only partially blocked by tolbutamide, which may also be an atypical KATP current. We conclude that KATP channels are expressed in normal DRG, but in very few neurons and only in nociceptors. [source] Taurocholic acid-induced secretion in normal and cystic fibrosis mouse ileumJOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 5 2001J. Hardcastle Bile acids cause secretion throughout the intestinal tract and this process contributes to maintaining the fluidity of intestinal contents. In cystic fibrosis (CF) defective intestinal secretion can lead to excessive dehydration of the luminal contents and the development of clinical symptoms. This study was designed to investigate bile acid-induced secretion in mouse ileum and to determine whether this process was defective in CF. Taurocholic acid-induced secretion was monitored as a rise in short-circuit current (SCC) in ileal sheets from normal (Swiss MF1) and transgenic CF mice. Taurocholic acid increased the SCC in both intact and stripped ileal sheets from Swiss MF1 mice. This effect was due to a stimulation of electrogenic Cl, secretion as it was inhibited by Cl, -free conditions, serosal furosemide (frusemide), mucosal diphenylamine-2-carboxylic acid (DPC) and increased serosal K+ concentration, without being affected by reduced mucosal Na+ concentration. Taurocholic acid-induced secretion was inhibited by tetrodotoxin, indicating the involvement of a neural pathway, but this did not include capsaicin-sensitive afferent neurons or muscarinic cholinoreceptors. Mucosal mast cells also contributed to the response. Responses in tissues from transgenic wild-type mice were similar to those obtained with Swiss MF1 animals, but ilea from CF mice exhibited a lower basal SCC with significantly reduced secretory responses to acetylcholine and taurocholic acid. We concluded that taurocholic acid induces ileal secretion by a mechanism that entails activation of enteric nerves and degranulation of mucosal mast cells. Impaired bile acid-induced secretion in CF may contribute to luminal dehydration. [source] Crops and genotypes differ in efficiency of potassium uptake and usePHYSIOLOGIA PLANTARUM, Issue 4 2008Zed Rengel Cultivars with increased efficiency of uptake and utilization of soil nutrients are likely to have positive environmental effects through reduced usage of chemicals in agriculture. This review assesses the available literature on differential uptake and utilization efficiency of K in farming systems. Large areas of agricultural land in the world are deficient in K (e.g. 3/4 of paddy soils in China, 2/3 of the wheatbelt in Southern Australia), with export in agricultural produce (especially hay) and leaching (especially in sandy soils) contributing to lowering of K content in the soil. The capacity of a genotype to grow and yield well in soils low in available K is K efficiency. Genotypic differences in efficiency of K uptake and utilization have been reported for all major economically important plants. The K-efficient phenotype is a complex one comprising a mixture of uptake and utilization efficiency mechanisms. Differential exudation of organic compounds to facilitate release of non-exchangeable K is one of the mechanisms of differential K uptake efficiency. Genotypes efficient in K uptake may have a larger surface area of contact between roots and soil and increased uptake at the root,soil interface to maintain a larger diffusive gradient towards roots. Better translocation of K into different organs, greater capacity to maintain cytosolic K+ concentration within optimal ranges and increased capacity to substitute Na+ for K+ are the main mechanisms underlying K utilization efficiency. Further breeding for increased K efficiency will be dependent on identification of suitable markers and compounding of efficiency mechanisms into locally adapted germplasm. [source] The plasma membrane Na+/H+ antiporter SOS1 is essential for salt tolerance in tomato and affects the partitioning of Na+ between plant organsPLANT CELL & ENVIRONMENT, Issue 7 2009RAQUEL OLĶAS ABSTRACT We have identified a plasma membrane Na+/H+ antiporter gene from tomato (Solanum lycopersicum), SlSOS1, and used heterologous expression in yeast to confirm that SlSOS1 was the functional homolog of AtSOS1. Using post-transcriptional gene silencing, we evaluated the role played by SlSOS1 in long-distance Na+ transport and salt tolerance of tomato. Tomato was used because of its anatomical structure, more complex than that of Arabidopsis, and its agricultural significance. Transgenic tomato plants with reduced expression of SlSOS1 exhibited reduced growth rate compared to wild-type (WT) plants in saline conditions. This sensitivity correlated with higher accumulation of Na+ in leaves and roots, but lower contents in stems of silenced plants under salt stress. Differential distribution of Na+ and lower net Na+ flux were observed in the xylem sap in the suppressed plants. In addition, K+ concentration was lower in roots of silenced plants than in WT. Our results demonstrate that SlSOS1 antiporter is not only essential in maintaining ion homeostasis under salinity, but also critical for the partitioning of Na+ between plant organs. The ability of tomato plants to retain Na+ in the stems, thus preventing Na+ from reaching the photosynthetic tissues, is largely dependent on the function of SlSOS1. [source] NaCl-induced changes in cytosolic free Ca2+ in Arabidopsis thaliana are heterogeneous and modified by external ionic compositionPLANT CELL & ENVIRONMENT, Issue 8 2008FRANCES E. TRACY ABSTRACT Increases in cytosolic free Ca2+ ([Ca2+]cyt) are common to many stress-activated signalling pathways, including the response to saline environments. We have investigated the nature of NaCl-induced [Ca2+]cyt signals in whole Arabidopsis thaliana seedlings using aequorin. We found that NaCl-induced increases in [Ca2+]cyt are heterogeneous and mainly restricted to the root. Both the concentration of NaCl and the composition of the solution bathing the root have profound effects on the magnitude and dynamics of NaCl-induced increases in [Ca2+]cyt. Alteration of external K+ concentration caused changes in the temporal and spatial pattern of [Ca2+]cyt increase, providing evidence for Na+ -induced Ca2+ influx across the plasma membrane. The effects of various pharmacological agents on NaCl-induced increases in [Ca2+]cyt indicate that NaCl may induce influx of Ca2+ through both plasma membrane and intracellular Ca2+ -permeable channels. Analysis of spatiotemporal [Ca2+]cyt dynamics using photon-counting imaging revealed additional levels of complexity in the [Ca2+]cyt signal that may reflect the oscillatory nature of NaCl-induced changes in single cells. [source] A voltage-dependent K+ current contributes to membrane potential of acutely isolated canine articular chondrocytesTHE JOURNAL OF PHYSIOLOGY, Issue 1 2004Jim R. Wilson The electrophysiological properties of acutely isolated canine articular chondrocytes have been characterized using patch-clamp methods. The ,steady-state' current,voltage relationship (I,V) of single chondrocytes over the range of potentials from ,100 to +40 mV was highly non-linear, showing strong outward rectification positive to the zero-current potential. Currents activated at membrane potentials negative to ,50 mV were time independent, and the I,V from ,100 to ,60 mV was linear, corresponding to an apparent input resistance of 9.3 ± 1.4 G, (n= 23). The outwardly rectifying current was sensitive to the K+ channel blocking ion tetraethylammonium (TEA), which had a 50% blocking concentration of 0.66 mm (at +50 mV). The ,TEA-sensitive' component of the outwardly rectifying current had time- and membrane potential-dependent properties, activated near ,45 mV and was half-activated at ,25 mV. The reversal potential of the ,TEA-sensitive' current with external K+ concentration of 5 mm and internal concentration of 145 mm, was ,84 mV, indicating that the current was primarily carried by K+ ions. The resting membrane potential of isolated chondrocytes (,38.1 ± 1.4 mV; n= 19) was depolarized by 14.8 ± 0.9 mV by 25 mm TEA, which completely blocked the K+ current of these cells. These data suggest that this voltage-sensitive K+ channel has an important role in regulating the membrane potential of canine articular chondrocytes. [source] Changes in extracellular K+ concentration modulate contractility of rat and rabbit cardiac myocytes via the inward rectifier K+ current IK1THE JOURNAL OF PHYSIOLOGY, Issue 3 2004Ron Bouchard The mechanisms underlying the inotropic effect of reductions in [K+]o were studied using recordings of membrane potential, membrane current, cell shortening and [Ca2+]i in single, isolated cardiac myocytes. Three types of mammalian myocytes were chosen, based on differences in the current density and intrinsic voltage dependence of the inwardly rectifying background K+ current IK1 in each cell type. Rabbit ventricular myocytes had a relatively large IK1 with a prominent negative slope conductance whereas rabbit atrial cells expressed much smaller IK1, with little or no negative slope conductance. IK1 in rat ventricle was intermediate in both current density and slope conductance. Action potential duration is relatively short in both rabbit atrial and rat ventricular myocytes, and consequently both cell types spend much of the duty cycle at or near the resting membrane potential. Rapid increases or decreases of [K+]o elicited significantly different inotropic effects in rat and rabbit atrial and ventricular myocytes. Voltage-clamp and current-clamp experiments showed that the effects on cell shortening and [Ca2+]i following changes in [K+]o were primarily the result of the effects of alterations in IK1, which changed resting membrane potential and action potential waveform. This in turn differentially altered the balance of Ca2+ efflux via the sarcolemmal Na+,Ca2+ exchanger, Ca2+ influx via voltage-dependant Ca2+ channels and sarcoplasmic reticulum (SR) Ca2+ release in each cell type. These results support the hypothesis that the inotropic effect of alterations of [K+]o in the heart is due to significant non-linear changes in the current,voltage relation for IK1 and the resulting modulation of the resting membrane potential and action potential waveform. [source] External K+ modulates the activity of the Arabidopsis potassium channel SKOR via an unusual mechanismTHE PLANT JOURNAL, Issue 2 2006Ingela Johansson Summary Plant outward-rectifying K+ channels mediate K+ efflux from guard cells during stomatal closure and from root cells into the xylem for root,shoot allocation of potassium (K). Intriguingly, the gating of these channels depends on the extracellular K+ concentration, although the ions carrying the current are derived from inside the cell. This K+ dependence confers a sensitivity to the extracellular K+ concentration ([K+]) that ensures that the channels mediate K+ efflux only, regardless of the [K+] prevailing outside. We investigated the mechanism of K+ -dependent gating of the K+ channel SKOR of Arabidopsis by site-directed mutagenesis. Mutations affecting the intrinsic K+ dependence of gating were found to cluster in the pore and within the sixth transmembrane helix (S6), identifying an ,S6 gating domain' deep within the membrane. Mapping the SKOR sequence to the crystal structure of the voltage-dependent K+ channel KvAP from Aeropyrum pernix suggested interaction between the S6 gating domain and the base of the pore helix, a prediction supported by mutations at this site. These results offer a unique insight into the molecular basis for a physiologically important K+ -sensory process in plants. [source] Effect of rearing density on the growth and welfare indices of juvenile spotted wolffish, Anarhichas minor (Olafsen)AQUACULTURE RESEARCH, Issue 8 2010Sarah Tremblay-Bourgeois Abstract The goal of this study was to determine the optimal stocking density for rearing juvenile spotted wolffish, Anarhichas minor (Olafsen), at two different sizes and assess the welfare status in relation to density. No major growth impairment was observed, although smaller fish (50,100 g) were significantly affected by density during the 120 days of the experiment, with final mean weights of 119.6 ± 11.6, 118.0 ± 5.8 and 88.7 ± 0.6 g for initial rearing densities of 10, 20 and 40 kg m,2 respectively. No effect of rearing density was seen for larger fish (100,160 g) during the 90 days of the experiment, with final mean weights of 160.2 ± 5.9, 159.7 ± 3.7 and 163.7 ± 11.5 g at fixed rearing densities of 20, 30 and 40 kg m,2 respectively. Our results suggest that the optimal rearing density of juvenile spotted wolffish is below 40 kg m,2 for smaller size fish (,50,100 g) and probably ,40 kg m,2 for the larger fish (100,160 g). Furthermore, it appears that the range of rearing density used did not have a significant effect on a selection of stress indicators (Na+ and K+ concentration, haematocrit, hepatosomatic index, total amount of plasma proteins and liver and muscle water content) and immunity response (plasma lysozyme activity) of juvenile spotted wolffish, making it a very tolerant species to crowding. [source] Milt characteristics of diploid and triploid Atlantic cod (Gadus morhua L.)AQUACULTURE RESEARCH, Issue 10 2009Stefano Peruzzi Abstract The work compares the characteristics of milt produced by diploid and triploid Atlantic cod in terms of sperm motility, density, DNA content, seminal-fluid composition and the ability of sperm to fertilize the eggs. The mean track velocity (VCL) was higher in the sperm of diploid than in the triploid males at 20 s post-activation (p.a.; 124.04 ± 6.91 vs. 113.32 ± 6.32 ,m s,1), but not at 40 s p.a. No differences between ploidies were observed for the remaining sperm-motility descriptors as for spermatozoa density, spermatocrit or seminal fluid's variables like pH, osmolarity, Cl,, Na+, Ca2+ and K+ concentration. Triploid males produced aneuploid sperm cells (average 1.46n, range 1.2,1.6n) and the larvae generated from artificial crossings with diploid females showed abnormal morphology and did not survive to exogenous feeding. Plasma concentration of 11-ketotestosterone in sexually mature diploid and triploid males was similar (5.35 ± 1.54 vs. 4.82 ± 1.15 ng mL,1) and no differences were found in the ability of males of both ploidies to induce spawning when held in tanks with diploid females. The paper provides evidence of gametic sterility of triploid males and examines the use of triploid fish as a management option to address the issues of genetic containment of farmed cod alongside measures for securing present fish-farming technologies. [source] Cage colour and post-harvest K+ concentration affect skin colour of Australian snapper Pagrus auratus (Bloch & Schneider, 1801)AQUACULTURE RESEARCH, Issue 9 2008Ben J Doolan Abstract In an attempt to improve post-harvest skin colour in cultured Australian snapper Pagrus auratus, a two-factor experiment was carried out to investigate the effects of a short-term change in cage colour before harvest, followed by immersion in K+ -enriched solutions of different concentrations. Snapper supplemented with 39 mg unesterified astaxanthin kg,1 for 50 days were transferred to black (for 1 day) or white cages (for 1 or 7 days) before euthanasia by immersing fish in seawater ice slurries supplemented with 0, 150, 300, 450 or 600 mmol L,1 K+ for 1 h. Each treatment was replicated with five snapper (mean weight=838 g) held individually within 0.2 m3 cages. L*, a* and b* skin colour values of all fish were measured after removal from K+ solutions at 0, 3, 6, 12, 24 and 48 h. After immersion in K+ solutions, fish were stored on ice. Both cage colour and K+ concentration significantly affected post-harvest skin colour (P<0.05), and there was no interaction between these factors at any of the measurement times (P>0.05). Conditioning dark-coloured snapper in white surroundings for 1 day was sufficient to significantly improve skin lightness (L*) after death. Although there was no difference between skin lightness values for fish held for either 1 or 7 days in white cages at measurement times up to 12 h, fish held in white cages for 7 days had significantly higher L* values (i.e. they were lighter) after 24 and 48 h of storage on ice than those held only in white cages for 1 day. K+ treatment also affected (improved) skin lightness post harvest although not until 24 and 48 h after removal of fish from solutions. Before this time, K+ treatment had no effect on skin lightness. Snapper killed by seawater ice slurry darkened (lower L*) markedly during the first 3 h of storage in contrast with all K+ treatments that prevented darkening. After 24 and 48 h of storage on ice, fish exposed to 450 and 600 mmol L,1 K+ were significantly lighter than fish from seawater ice slurries. In addition, skin redness (a*) and yellowness (b*) were strongly dependent on K+ concentration. The initial decline in response to K+ was overcome by a return of a* and b* values with time, most likely instigated by a redispersal of erythrosomes in skin erythrophores. Fish killed with 0 mmol L,1 K+ maintained the highest a* and b* values after death, but were associated with darker (lower L*) skin colouration. It is concluded that a combination of conditioning snapper in white surroundings for 1 day before harvest, followed by immersion in seawater ice slurries supplemented with 300,450 mmol L,1 K+ improves skin pigmentation after >24 h of storage on ice. [source] The Effects of Angiotensin Converting Enzyme Inhibitors on Potassium Homeostasis in Dialysis Patients With and Without Residual Renal FunctionARTIFICIAL ORGANS, Issue 8 2009Elizabeth Garthwaite Abstract Hyperkalemia is exacerbated by angiotensin converting enzyme inhibitors (ACE-I). Distal potassium (K+) secretion is negligible in anuric patients. ACE-I therapy may reduce renal, peritoneal, and colonic K+ losses. We examined the effect of ACE-I therapy on serum, urinary, and dialysate K+ in a cross-section of peritoneal and hemodialysis patients. Serum, 24-h urine K+, and peritoneal dialysate excretion K+ levels were measured and the results were compared in the various dialysis and treatment groups. Eighty-one hemodialysis (HD) and 32 peritoneal dialysis (PD) patients were included. Serum K+ in HD patients with no residual renal function (RRF) was higher in those receiving ACE-I therapy (P = 0.02). Serum K+ levels in HD patients receiving ACE-I treatments with RRF was similar to that in oligoanuric HD patients not receiving an ACE-I. Urinary K+ excretion was significantly reduced in those on ACE-I therapy versus those not on an ACE-I (P < 0.05). Mean serum K+ was lower in PD versus HD patients (P < 0.05). PD patients with no RRF on ACE-I therapy had higher serum K+ concentrations (P = 0.002) and dialysate K+ excretion was lower (P = 0.05), in comparison with PD patients not on an ACE-I. PD patients with RRF on ACE-I therapy had higher serum K+ concentrations compared with those not on ACE-I therapy (P = 0.03). Both urinary and dialysate K+ excretion were reduced (P = 0.001 and P = 0.002, respectively). ACE-I therapy increases serum K+ concentration in dialysis patients. PD patients have relatively lower serum K+ levels compared with HD patients. In PD patients, ACE-I therapy reduces dialysate K+. These changes may result from reduced peritoneal movement of K+. [source] Glutamate-induced post-activation inhibition of locus coeruleus neurons is mediated by AMPA/kainate receptors and sodium-dependent potassium currentsBRITISH JOURNAL OF PHARMACOLOGY, Issue 4 2009Teresa Zamalloa Background and purpose:, Locus coeruleus (LC) neurons respond to sensory stimuli with a glutamate-triggered burst of spikes followed by an inhibition. The aim of our work was to characterize the inhibitory effect of glutamate in the LC. Experimental approach:, Single-unit extracellular and patch-clamp recordings were performed to examine glutamate responses in rat brain slices containing the LC. Key results:, Glutamate caused an initial activation followed by a late post-activation inhibition (PAI). Both effects were blocked by an AMPA/kainate receptor antagonist but not by NMDA or metabotropic glutamate receptor antagonists. All glutamate receptor agonists were able to activate neurons, but only AMPA and quisqualate caused inhibition. In neurons clamped at ,60 mV, glutamate and AMPA induced inward, followed by outward, currents, with the latter reversing polarity at ,110 mV. Glutamate-induced PAI was not modified by ,2 -adrenoceptor, µ opioid, A1 adenosine and GABAA/B receptor antagonists or Ca2+ -dependent release blockade, but it was reduced by raising the extracellular K+ concentration. Glutamate-induced PAI was not affected by several potassium channel, Na+/K+ pump, PKC and neuronal NO synthase inhibitors or lowering the extracellular Ca2+ concentration. The Na+ -activated K channel opener bithionol concentration-dependently potentiated glutamate-induced PAI, whereas partial (80%) Na+ replacement reduced glutamate- and AMPA-induced PAI. Finally, reverse transcription polymerase chain reaction assays showed the presence of mRNA for the Ca2+ -impermeable GluR2 subunit in the LC. Conclusions and implications:, Glutamate induces a late PAI in the LC, which may be mediated by a novel postsynaptic Na+ -dependent K+ current triggered by AMPA/kainate receptors. Mandarin translation of abstract [source] Pre-steady state kinetics of ATP hydrolysis by Na,K-ATPaseCELL BIOCHEMISTRY AND FUNCTION, Issue 3 2009Nikhat Manzoor Abstract Fast reaction kinetics of ATP hydrolysis by Na,K-ATPase has been investigated by following absorption pattern of pH sensitive dye in stopped flow spectrophotometer. Distinct pre-steady state phase signal could be recorded with an initial decrease in acidity followed by increase in acidity. Average half time for H+ absorption and peak alkalinity was, respectively, 30,ms and 60,ms. Under optimal Na+ (120,mM) and K+ (30,mM) concentrations, magnitude of both H+ absorption and H+ release are found to be about 1.0,H+/ATPase molecule. H+ absorption and release decreased with decrease in Na+ concentration, H+ release was more affected. Both H+ absorption and H+ release are found to be independent of K+ concentration in the pre-steady state phase. No H+ absorption or release was observed following mixing of either ADP, Na+ or K+ alone with ATPase. Effect of delayed mixing of Na+ or K+ on two phases of pre-steady state cycle indicates that ATP hydrolytic cycle starts without K+ ions if optimal Na+ is present. ATP hydrolytic cycle does not start in the absence of Na+ ions. Results obtained have been interpreted in terms of an extended kinetic scheme for Na,K-ATPase. Copyright © 2009 John Wiley & Sons, Ltd. [source] Using Diffusion NMR To Characterize Guanosine Self-Association: Insights into Structure and MechanismCHEMISTRY - A EUROPEAN JOURNAL, Issue 1 2005Mark S. Kaucher Abstract This paper presents results from a series of pulsed field gradient (PFG) NMR studies on lipophilic guanosine nucleosides that undergo cation-templated assembly in organic solvents. The use of PFG-NMR to measure diffusion coefficients for the different aggregates allowed us to observe the influences of cation, solvent and anion on the self-assembly process. Three case studies are presented. In the first study, diffusion NMR confirmed formation of a hexadecameric G-quadruplex [G,1]16,4,K+,4,pic, in CD3CN. Furthermore, hexadecamer formation from 5,-TBDMS-2,,3,-isopropylidene G,1 and K+ picrate was shown to be a cooperative process in CD3CN. In the second study, diffusion NMR studies on 5,-(3,5-bis(methoxy)benzoyl)-2,,3,-isopropylidene G,4 showed that hierarchical self-association of G8 -octamers is controlled by the K+ cation. Evidence for formation of both discrete G8 -octamers and G16 -hexadecamers in CD2Cl2 was obtained. The position of this octamer,hexadecamer equilibrium was shown to depend on the K+ concentration. In the third case, diffusion NMR was used to determine the size of a guanosine self-assembly where NMR signal integration was ambiguous. Thus, both diffusion NMR and ESI-MS show that 5,- O -acetyl-2,,3,- O -isopropylidene G,7 and Na+ picrate form a doubly charged octamer [G,7]8,2,Na+,2,pic,9 in CD2Cl2. The anion's role in stabilizing this particular complex is discussed. In all three cases the information gained from the diffusion NMR technique enabled us to better understand the self-assembly processes, especially regarding the roles of cation, anion and solvent. [source] Effects of ouabain on contractions induced by manganese ions in Ca2+ -free, isotonic solutions with varying concentrations of K+ in guinea-pig taenia coliFUNDAMENTAL & CLINICAL PHARMACOLOGY, Issue 3 2005Tetsuyuki Nasu Abstract The action of ouabain, a cell membrane Na+, K+ -ATPase blocker, on contractions induced by manganese ions (Mn2+) in Ca2+ -free, isotonic solutions with varying concentrations of K+ in the external medium were investigated in order to evaluate the underlying role of external Na+ in Mn2+ -induced contractions in isolated taenia coli of the guinea-pig. Mn2+ at 5 mm induced greater contractions as external isotonic K+ concentrations progressively increased from 10 to 100 mm. Ouabain (2 × 10,4 m) completely inhibited tension development stimulated by 5 mm Mn2+ in isotonic, 30 mm K+ (96 mm Na+) medium. Whereas, the tension inhibitory effects of ouabain became progressively weaker as isotonic, external K+ concentrations increased to 60 mm, which successively decreased external Na+ concentrations. Eventually, ouabain failed to affect contractions stimulated by Mn2+ in isotonic, 126 mm K+, Na+ -deficient medium. Ouabain caused progressively greater increase in cellular Na+ concentrations as the Na+ concentrations increased in the isotonic, K+ medium. While, pyruvate, which penetrates cell independently of external Na+, reversed the inhibition of tension by ouabain in isotonic, 30 mm K+, Na+ -sufficient (96 mm) medium containing 5 mm Mn2+. These results suggested that Mn2+ induced the contraction, which was maintained by glucose transport depending on external Na+, in the case of Na+ -sufficient medium in K+ -depolarized taenia coli. However, it induced the contraction independent of external Na+, in the case of Na+ -deficient, K+ medium. Ouabain might exhibit greater inhibition of the contraction induced by Mn2+ as the decrease in the Na+ gradient across the cell membranes continues. [source] Mechanisms of glutamate release elicited in rat cerebrocortical nerve endings by ,pathologically' elevated extraterminal K+ concentrationsJOURNAL OF NEUROCHEMISTRY, Issue 3 2007Luca Raiteri Abstract Extracellular [K+] can increase during some pathological conditions, resulting into excessive glutamate release through multiple mechanisms. We here investigate the overflow of [3H]d -aspartate ([3H] d -ASP) and of endogenous glutamate elicited by increasing [K+] from purified rat cerebrocortical synaptosomes. Depolarization with [K+] , 15 mmol/L provoked [3H] d -ASP and glutamate overflows almost totally dependent on external Ca2+. Consistent with release by exocytosis, the overflow of [3H] d -ASP evoked by 12 mmol/L K+ was sensitive to clostridial toxins. The overflows evoked by 35/50 mmol/L K+ remained external Ca2+ -dependent by more than 50%. The Ca2+ -independent components of the [3H] d -ASP overflows evoked by [K+] > 15 mmol/L were prevented by the glutamate transporter inhibitors dl - threo -beta-benzyloxyaspartate (dl -TBOA) and dihydrokainate. Differently, the overflows of endogenous glutamate provoked by [K+] > 15 mmol/L were insensitive to both inhibitors; the external Ca2+ -independent glutamate overflow caused by 50 mmol/L KCl was prevented by bafilomycin, by chelating intraterminal Ca2+, by blocking the mitochondrial Na+/Ca2+ exchanger and, for a small portion, by blocking anion channels. In contrast to purified synaptosomes, the 50 mmol/L K+ -evoked release of endogenous glutamate or [3H]D-ASP was inhibited by dl -TBOA in crude synaptosomes; moreover, it was external Ca2+ -insensitive and blocked by dl -TBOA in purified gliosomes, suggesting that carrier-mediated release of endogenous glutamate provoked by excessive [K+] in CNS tissues largely originates from glia. [source] The cyclic nucleotide-gated channel, AtCNGC10, influences salt tolerance in ArabidopsisPHYSIOLOGIA PLANTARUM, Issue 3 2008Kun-Mei Guo Cyclic nucleotide-gated channels (CNGCs) in the plasma membrane transport K+ and other cations; however, their roles in the response and adaptation of plants to environmental salinity are unclear. Growth, cation contents, salt tolerance and K+ fluxes were assessed in wild-type and two AtCNGC10 antisense lines (A2 and A3) of Arabidopsis thaliana (L.) Heynh. Compared with the wild-type, mature plants of both antisense lines had altered K+ and Na+ concentrations in shoots and were more sensitive to salt stress, as assessed by biomass and Chl fluorescence. The shoots of A2 and A3 plants contained higher Na+ concentrations and significantly higher Na+/K+ ratios compared with wild-type, whereas roots contained higher K+ concentrations and lower Na+/K+ ratios. Four-day-old seedlings of both antisense lines exposed to salt stress had smaller Na+/K+ ratios and longer roots than the wild-type. Under sudden salt treatment, the Na+ efflux was higher and the K+ efflux was smaller in the antisense lines, indicating that AtCNGC10 might function as a channel providing Na+ influx and K+ efflux at the root/soil interface. We conclude that the AtCNGC10 channel is involved in Na+ and K+ transport during cation uptake in roots and in long-distance transport, such as phloem loading and/or xylem retrieval. Mature A2 and A3 plants became more salt sensitive than wild-type plants because of impaired photosynthesis induced by a higher Na+ concentration in the leaves. [source] Cellular mechanisms of potassium transport in plantsPHYSIOLOGIA PLANTARUM, Issue 4 2008Dev T. Britto Potassium (K+) is the most abundant ion in the plant cell and is required for a wide array of functions, ranging from the maintenance of electrical potential gradients across cell membranes, to the generation of turgor, to the activation of numerous enzymes. The majority of these functions depend more or less directly upon the activities and regulation of membrane-bound K+ transport proteins, operating over a wide range of K+ concentrations. Here, we review the physiological aspects of potassium transport systems in the plasma membrane, re-examining fundamental problems in the field such as the distinctions between high- and low-affinity transport systems, the interactions between K+ and other ions such as NH4+ and Na+, the regulation of cellular K+ pools, the generation of electrical potentials and the problems involved in measurement of unidirectional K+ fluxes. We place these discussions in the context of recent discoveries in the molecular biology of K+ acquisition and produce an overview of gene families encoding K+ transporters. [source] Electrophysiological characterization of pathways for K+ uptake into growing and non-growing leaf cells of barleyPLANT CELL & ENVIRONMENT, Issue 12 2009VADIM VOLKOV ABSTRACT Potassium is a major osmolyte used by plant cells. The accumulation rates of K+ in cells may limit the rate of expansion. In the present study, we investigated the involvement of ion channels in K+ uptake using patch clamp technique. Ion currents were quantified in protoplasts of the elongation and emerged blade zone of the developing leaf 3 of barley (Hordeum vulgare L.). A time-dependent inward-rectifying K+ -selective current was observed almost exclusively in elongation zone protoplasts. The current showed characteristics typical of Shaker-type channels. Instantaneous inward current was highest in the epidermis of the emerged blade and selective for Na+ over K+. Selectivity disappeared, and currents decreased or remained the same, depending on tissue, in response to salt treatment. Net accumulation rates of K+ in cells calculated from patch clamp current,voltage curves exceeded rates calculated from membrane potential and K+ concentrations of cells measured in planta by factor 2.5,2.7 at physiological apoplastic K+ concentrations (10,100 mm). It is concluded that under these conditions, K+ accumulation in growing barley leaf cells is not limited by transport properties of cells. Under saline conditions, down-regulation of voltage-independent channels may reduce the capacity for growth-related K+ accumulation. [source] Root structure and cellular chloride, sodium and potassium distribution in salinized grapevinesPLANT CELL & ENVIRONMENT, Issue 6 2003R. STOREY ABSTRACT X-ray microanalysis was used to study the patterns of K+, Na+ and Cl, accumulation in salinized (25 mm NaCl) and non-salinized grapevine (Vitis) roots. The aim was to determine whether NaCl affects patterns of Cl, accumulation differentially in the roots of a Cl, -excluding genotype and a non-excluding genotype. Two regions of fibrous roots were analysed: (1) a region 2,3 mm basipetal to the root tip; and (2) a region of the root 10,12 mm basipetal to the root tip where the outermost layer is the hypodermis. The ion contents of the hypodermis, cortex, endodermis and pericycle vacuoles were analysed. Data were also collected from the cytoplasm of the endodermal and pericycle cells. The analyses showed that the ion profiles of the hypodermis and the endodermis were significantly different from those of the cortex and pericycle. The hypodermis and endodermis had higher K+ and lower Na+ and Cl, than surrounding cells. Some changes due to salinity such as increased K+ concentrations in the hypodermis were also noted. Chloride concentrations did not differ between the genotypes in the hypodermis, across the cortex or in the endodermis, but were higher in the pericycle of the excluder in comparison with the non-excluding genotype. However, K+/Na+ ratios of the cortex and endodermis were higher in the excluder. The pericycle cells exhibited the greatest ability to sequester Na+ and Cl, in vacuoles. Overall the data show cell-type-specific ion accumulation patterns and small but significant differences were found between genotypes. The possibility that these accumulation patterns arise from differences in uptake properties of cell types and/or result from the spatial distribution of the cell types along the competing symplastic and apoplastic ion transport pathways across the root is discussed. [source] The Effects of Angiotensin Converting Enzyme Inhibitors on Potassium Homeostasis in Dialysis Patients With and Without Residual Renal FunctionARTIFICIAL ORGANS, Issue 8 2009Elizabeth Garthwaite Abstract Hyperkalemia is exacerbated by angiotensin converting enzyme inhibitors (ACE-I). Distal potassium (K+) secretion is negligible in anuric patients. ACE-I therapy may reduce renal, peritoneal, and colonic K+ losses. We examined the effect of ACE-I therapy on serum, urinary, and dialysate K+ in a cross-section of peritoneal and hemodialysis patients. Serum, 24-h urine K+, and peritoneal dialysate excretion K+ levels were measured and the results were compared in the various dialysis and treatment groups. Eighty-one hemodialysis (HD) and 32 peritoneal dialysis (PD) patients were included. Serum K+ in HD patients with no residual renal function (RRF) was higher in those receiving ACE-I therapy (P = 0.02). Serum K+ levels in HD patients receiving ACE-I treatments with RRF was similar to that in oligoanuric HD patients not receiving an ACE-I. Urinary K+ excretion was significantly reduced in those on ACE-I therapy versus those not on an ACE-I (P < 0.05). Mean serum K+ was lower in PD versus HD patients (P < 0.05). PD patients with no RRF on ACE-I therapy had higher serum K+ concentrations (P = 0.002) and dialysate K+ excretion was lower (P = 0.05), in comparison with PD patients not on an ACE-I. PD patients with RRF on ACE-I therapy had higher serum K+ concentrations compared with those not on ACE-I therapy (P = 0.03). Both urinary and dialysate K+ excretion were reduced (P = 0.001 and P = 0.002, respectively). ACE-I therapy increases serum K+ concentration in dialysis patients. PD patients have relatively lower serum K+ levels compared with HD patients. In PD patients, ACE-I therapy reduces dialysate K+. These changes may result from reduced peritoneal movement of K+. [source] Four new cases of stomatin-deficient hereditary stomatocytosis syndrome: association of the stomatin-deficient cryohydrocytosis variant with neurological dysfunctionBRITISH JOURNAL OF HAEMATOLOGY, Issue 6 2004Britta Fricke Summary This report concerns congenitally Na+,K+ leaky red cells of the ,hereditary stomatocytosis' class. Three new isolated cases and one new pedigree are described, and one previously reported case is expanded. In all cases, Western blotting of red cell membranes revealed a deficiency in the 32 kDa membrane protein, stomatin. All showed pronounced cation leaks at 37°C with markedly abnormal intracellular Na+ and K+ concentrations, like all other such stomatin-deficient cases. Consistent with recent findings in two previously described British pedigrees, immunocytochemistry demonstrated that the deficiency of stomatin was not complete. On typical blood films, some red cells showed positive stomatin immunoreactivity, while most were negative, although in one case only a minority were negative. All platelets and neutrophils were stomatin positive. The cases differed markedly between themselves with regard to the temperature dependence of the passive leak to K+. Three showed a simple monotonic temperature dependence, while two showed a minimum at around 20,25°C, such that the cells were extremely leaky at 0°C, giving the phenotype known as ,cryohydrocytosis'. These patients are the only two known cases of stomatin-deficient cryohydrocytosis. Both showed a congenital syndrome of mental retardation, seizures, cataracts and massive hepatosplenomegaly, probably defining a new haemato-neurological syndrome. [source] Effect of K+ and Rb+ on the action of verapamil on a voltage-gated K+ channel, hKv1.3: implications for a second open state?BRITISH JOURNAL OF PHARMACOLOGY, Issue 5 2009Z Kuras Background and purpose:, Verapamil blocks current through the voltage-gated K+ channel Kv1.3 in the open and inactivated state of the channel but not the closed state. The binding site for verapamil was proposed to be close to the selectivity filter and the occupancy of the selectivity filter might therefore influence verapamil affinity. Experimental approach:, We investigated the influence of intra- and extracellular K+ and Rb+ on the effect of verapamil by patch-clamp studies, in COS-7 cells transfected with hKv1.3 channels. Key results:, Verapamil affinity was highest in high intracellular K+ concentrations ([K+]i) and lowest in low [Rb+]i, indicating an influence of intracellular cations on verapamil affinity. Experiments with a mutant channel (H399T), exhibiting a strongly reduced C-type inactivated state, demonstrated that part of this changed verapamil affinity in wild-type channels could be caused by altered C-type inactivation. External K+ and Rb+ could influence verapamil affinity by a voltage-dependent entry into the channel thereby modifying the verapamil off-rate and in addition causing a voltage-dependent verapamil off-rate. Conclusions and implications:, Recovery from verapamil block was mainly due to the voltage-dependent closing of channels (state-dependent block), implying a second open state of the channel. This hypothesis was confirmed by the dependency of the tail current time course on duration of the prepulse. We conclude that the wild-type hKv1.3 channel undergoes at least two different conformational changes before finally closing with a low verapamil affinity in one open state and a high verapamil affinity in the other open state. [source] | |||||||||||||||||||||||||