Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Barium Compounds”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,441 records · Page 80Linked to original sources
PubMed2001

100 years after grignard: where does the organometallic chemistry of the heavy alkaline Earth metals stand today?

Even a century after the discovery of the Grignard reagents, similar compounds of the heavy alkaline earth metals are still lacking. Owing to the industrial need for such compounds (in particular as anionic polymerization catalysts), the last few years have been marked by a rapid, extensive development which has culminated in the first structurally characterized alkylbarium derivatives such as the crown ether complex of bis(triphenylmethyl)barium (1). hmpt=hexamethylphosphoric acid triamide.

Grignard reactions↗
PubMed1985

Barium action potentials in regenerating axons of the lamprey spinal cord.

Intracellular recordings were obtained from growing tips of regenerating giant axons in the lamprey spinal cord, the recording sites verified by Lucifer yellow injection. In the presence of extracellular Ba++ (3-6 mM), tetraethylammonium (10-15 mM), and 4-aminopyridine (4-6 mM), action potentials showed prolonged plateaus. The fast initial phase of the action potential, but not the plateau (Ba++-spike), was blocked by tetrodotoxin (10(-6) gm/ml). The Ba++ spike was associated with increased membrane conductance and could be terminated with hyperpolarizing current pulses. Normal axons did not generate similar Ba++ spikes. However, TTX-resistant, voltage-dependant conductance changes could be elicited in normal axons if much higher concentrations of Ba++ (18-30 mM) were used. Their rate of rise was slower than in regenerating axons (0.6 V/sec vs 3.2 V/sec; n = 5), and the response did not outlast the current pulse. The Ba++ responses in normal and regenerating axons were blocked by ions known to block voltage-gated Ca++ conductances (Co++, Ni++, or Cd++). Therefore, these spikes probably represent Ba++ entry through voltage-dependent Ca++ channels, suggesting the presence of a higher-than-average voltage-dependent Ca++ conductance in the growing axon. However, Ca++-dependent spikes could not be obtained under any conditions in either normal or regenerating axons. Simultaneous intracellular recordings from growth cones and axons indicated that the Ba++ spike was initiated, in most cases, at the growth cone. The Ba++ spikes were recorded in regenerating axons for as long as 50 days following cord transection and were not correlatable with the "dying-back" phenomenon in cut axons, which usually is over before day 6. The concept of a higher-than-average voltage-dependent Ca++ conductance in growing tips of regenerating axons is in agreement with the hypothesis that Ca++ is important in regeneration and that regeneration may be related to the process of chemical synaptic transmission.

4-Aminopyridine↗
PubMed1985

Calcium-dependent inward currents in voltage-clamped guinea-pig olfactory cortex neurones.

Guinea-pig olfactory cortex neurones in vitro (23 degrees C--25 degrees C) were voltage clamped by means of a single microelectrode sample-and-hold technique. In most Cs+-loaded neurones (in the presence of tetrodotoxin), membrane depolarization beyond -60 mV elicited inward currents, which had rapid activation kinetics. The steady-state current-voltage relationship was N-shaped with a region of negative slope conductance between - 50 mV and - 20 mV. The rate of inactivation varied according to the holding potential and the command potential. The inward currents were maintained when external Ca2+ was replaced by Ba2+, and were blocked by Cd2+, suggesting that Ca2+ was the principal charge carrier. The results demonstrate the existence of calcium current in olfactory cortex neurones.

Animals↗
PubMed1993

Plasmalemmal, voltage-dependent ionic currents from excitable pulvinar motor cells of Mimosa pudica.

Plasmalemmal ionic currents from excitable motor cells of the primary pulvinus of Mimosa pudica were investigated by patch-clamp techniques. In almost all of the enzymatically isolated protoplasts, a delayed rectifier potassium current was activated by depolarization, while no currents were detected upon hyperpolarization. This sustained outward current was reversibly blocked by Ba and TEA and serves to repolarize the membrane potential. Outward single channel currents that very likely underly the macroscopic outward potassium current had an elementary conductance of approximately 20 pS. In addition, in a few protoplasts held at hyperpolarized potentials, depolarization-activated transient inward currents were observed, and under current clamp, action potential-like responses were triggered by depolarizing current injections or by mechanical perturbations. The activation characteristics of both inward currents and spikes showed striking similarities compared to those of action potentials in situ.

Barium↗
PubMed1988

Ionic currents in avian granulosa cells.

Transmembrane ionic currents have been recorded in single granulosa cells from the laying hen using the whole-cell patch-clamp technique. Under voltage-clamp conditions, depolarizing voltage steps evoked currents composed of a fast inactivating inward component and a delayed outward component. The former was activated at voltages more positive than -50 mV and was fully inactivated within 500 ms. It was blocked by D600 (methoxyverapamil) and by cobalt, suggesting that it is a calcium current. The latter displayed inward rectification and did not inactivate during long duration pulses. It was blocked by tetraethylammonium indicating that it is a potassium current. This is the first evidence of the existence of potassium and calcium transmembrane currents in granulosa cells.

Animals↗
PubMed1994

The use of epidemiological concepts and techniques to discern factors associated with the nitrate concentration of well water on swine farms in the USA.

This epidemiological study investigates the relationship between various factors associated with swine farms and the nitrate concentration of well water in the USA. Through a random sampling procedure, 605 swine farms located in 18 states were selected for inclusion in this study. A total of 631 well water samples were collected from these farms and tested for a variety of elements and compounds. The concentrations of nitrate, nitrite, sulfate, chloride, sodium, potassium, ammonia, fluoride, bromide and lithium were determined by an ion chromatograph while an inductively coupled argon plasma emission spectrophotometer was used to determine the concentrations of calcium, magnesium, barium, zinc, iron and phosphate. Data concerning various farm factors were gathered via a personally administered questionnaire. The data were examined using both multiple linear regression and logistic regression. Results indicate that 53.6% (338/631) of the wells contained detectable levels of nitrate, 11.7% (74/631) had nitrate levels exceeding 45 ppm and 4.3% (27/631) exceeded 100 ppm. Logistic models demonstrated an association between nitrate concentrations > 45 ppm, increasing water potassium levels and wells < 100 ft deep. Nitrate levels > 100 ppm were related to increasing water concentrations of potassium, magnesium, barium and zinc, wells 6-10 years old, increasing distance from the study farm to the nearest cattle farm and a greater distance to the nearest waterway located off the study farm. A negative association was seen between nitrate concentrations > 100 ppm, the water level of sulfate, and the use of the same well to supply both the household and livestock. Multiple linear regression models revealed a positive association between increasing nitrate concentration and the water levels of chloride, calcium, zinc and the greater number of miles from the study farm to the nearest farm with cattle or sheep. A negative association was noted between the concentration of well water nitrate and the water levels of sulfate and ammonia, the use of water treatment, the number of miles to the nearest farm with poultry, the employment of water treatment and the use of the same well to supply water to both livestock and the household.

Agriculture↗
PubMed1983

Calcium-activated potassium channels in liver cells.

Activation of certain membrane receptors increases the concentration of Ca2+ in the cytosol of hepatocytes. Since in most species these cells possess a PK(Ca) mechanism, the outcome is a rise in PK. This can be blocked by quinine, apamin and certain neuromuscular blocking agents. The binding of labelled apamin to hepatocytes has been studied under physiological conditions, and the relationship between the binding sites and K+ channels is discussed. The physiological role of the PK(Ca) mechanism in hepatocytes is unclear, though it is largely responsible for 'adrenaline hyperkalaemia'.

Animals↗
PubMed1987

A ouabain-sensitive hyperpolarization in rat striatal neurones in vitro.

Intracellular recordings were made from rat striatal neurones in vitro. In the presence of intracellular caesium and extracellular tetraethylammonium chloride (TEA) (5 mM) and barium (3 mM), long-lasting plateau potentials developed followed by a prominent voltage independent hyperpolarization which lasted several seconds. A similar afterhyperpolarization was observed when calcium was replaced by barium. The afterhyperpolarization was reduced in a potassium free medium and reversibly abolished in a Na+-free solution or by cooling the slice to 21-24 degrees C. It was also irreversibly blocked by ouabain (50 microM). This hyperpolarization may therefore result from the activation of a Na+,K+-ATPase electrogenic pump.

Action Potentials↗
PubMed1991

Rapid interaction of tetraethylammonium with delayed K+ channel in mammalian brain neuron.

In order to study the rapidity of interaction between tetraethylammonium (TEA) and the delayed K+ channel of the mammalian brain neuron, TEA was applied to isolated rat hippocampal pyramidal neurons in a time-controlled sequence with a voltage step using a concentration clamp technique. TEA at a concentration of 30 mM, externally applied, started to decrease the delayed K+ current (IKD) without any detectable delay after the onset of the drug application. The inhibitory action of TEA reached a steady state within 10 ms while the full recovery from the inhibition required 20-30 ms after removing TEA from the external solution. Ba2+ at a concentration of 30 mM also reduced the IKD without any detectable delay. However, it took 40-60 s to reach the steady state of inhibition. Full recovery from the inhibition by Ba2+ was obtained around 60 s after removal of Ba2+ from the external solution. It is suggested that the interaction of TEA with the delayed K+ channel is much faster than that of Ba2+.

Animals↗
PubMed1989

A metabolically stable analog of 1,4,5-inositol trisphosphate activates a novel K+ conductance in pyramidal cells of the rat hippocampal slice.

IP(s)3, a metabolically stable analog of 1,4,5-inositol trisphosphate (IP3), inhibited action potential firing when injected into hippocampal pyramidal cells. This effect was associated with decreased input resistance, a more negative resting potential, outward rectification at depolarized potentials, and an afterhyperpolarization. The response to IP(s)3 was unaffected by antagonists of Na+, Ca2+, and Cl- conductances, but was sensitive to changes in extracellular K+ concentration. The IP(s)3-induced conductance was voltage-dependent, was activated in 10 ms with depolarization, and was blocked by extracellular Ba2+ or intracellular Ca2+ chelation. It was not suppressed by other K+ conductance antagonists. Thus, IP(s)3 may activate a novel K+ conductance in CA1 pyramidal cells. IP3 itself did not elicit this conductance, suggesting it may be rapidly metabolized in these cells.

Action Potentials↗
PubMed1989

Calcium channel block by cadmium in chicken sensory neurons.

Cadmium block of calcium channels was studied in chicken dorsal root ganglion cells by a whole-cell patch clamp that provides high time resolution. Barium ion was the current carrier, and the channel type studied had a high threshold of activation and fast deactivation (type FD). Block of these channels by 20 microM external Cd2+ is voltage dependent. Cd2+ ions can be cleared from blocked channels by stepping the membrane voltage (Vm) to a negative value. Clearing the channels is progressively faster and more complete as Vm is made more negative. Once cleared of Cd2+, the channels conduct transiently on reopening but reequilibrate with Cd2+ and become blocked within a few milliseconds. Cd2+ equilibrates much more slowly with closed channels, but at a holding potential of -80 mV virtually all channels are blocked at equilibrium. Cd2+ does not slow closing of the channels, as would be expected if it were necessary for Cd2+ to leave the channels before closing occurred. Instead, the data show unambiguously that the channel gate can close when the channel is Cd2+ occupied.

Animals↗
PubMed1979

Inhibition of intestinal smooth muscle contraction by surface-active alkyltrimethylammonium salts.

The effects of surface-active alkyltrimethylammonium salts (C10--C20) on the contractile activity of isolated rat jejunum and on the gastrointestinal motility in anaesthetized rats were studied. The surfactants caused a dose-dependent depression of spontaneous contractions and of acetyl-beta-methylcholine and BaCl2 induced contractions of isolated rat jejunum. The depressant activity of the surface-active alkyltrimethylammonium salts on smooth muscle contraction increased with an increase in the length of the alkyl chain to maximum activity at C16. It is suggested that the depressant activity of the surface-active alkyltrimethylammonium salts on smooth muscle contraction is due to a non-specific interaction of the surfactants with the cellmembrane of the muscle cells. No effect on gastric and intestinal motility in vivo was observed following intragastric or intraintestinal administrations of surface-active alkyltrimethylammonium salts. This lack of effect upon intraintestinal or intragastric administration probably depends on an inability of the surfactants to reach the site of action when administered from the mucosal side.

Acetylcholine↗
PubMed1969

Tetrodotoxin-resistant electric activity in presynaptic terminals.

1. The electric properties of the giant synapse in the stellate ganglion of the squid have been further investigated.2. During tetrodotoxin (TTX) paralysis, a local response can be elicited from the terminal parts of the presynaptic axons after intracellular injection of tetraethyl ammonium ions (TEA).3. The response is characterized by an action potential of variable size and duration, whose fall is often preceded by a prolonged plateau. The response, especially the duration of the plateau, is subject to ;fatigue' during repetitive stimulation.4. The TTX-resistant form of activity is localized in the region of the synaptic contacts, and shows a marked electrotonic decrement even within less than 1 mm from the synapse. It is found only on the afferent, not on the efferent, side of the synapse.5. During the plateau of the response, the membrane resistance is greatly reduced below its resting value.6. The response depends on presence of external calcium and increases in size and duration with the calcium concentration. Strontium and barium substitute effectively for calcium. Manganese and, to a lesser extent, magnesium, counteract calcium and reduce the response. The response also declines, and ultimately disappears, if sodium is withdrawn for long periods.7. The relation of the local TTX-resistant response to the influx of calcium ions and to the release of the synaptic transmitter is discussed.

Action Potentials↗
PubMed1985

A calcium-activated potassium current in motor nerve terminals of the mouse.

Local circuit currents involving presynaptic terminals were recorded by micro-electrodes inserted into the perineurium of nerves from the triangularis sterni muscle of the mouse. A transient outward current component was isolated by blocking the voltage-activated (delayed rectifier) K current by 3,4-diaminopyridine (3,4-DAP). The amplitude of this component depended on external K concentration and fell to zero at [K]o = 15 mM. Since it also depended on [Ca]o, it was identified as a Ca-activated K current (IK(Ca)). Tetraethylammonium (TEA) (2 mM), Ba (2 mM), Co (10 mM) and Mn (2.5 mM) blocked IK(Ca). IK(Ca) decayed to zero in approximately 12 ms and recovered from inactivation in about 100 ms. Ca current was enhanced in inverse proportion to the degree of IK(Ca) depression. The possible role of IK(Ca) in the process of neuromuscular facilitation is briefly discussed.

4-Aminopyridine↗
PubMed1995

Effects of Ca2+ and K+ channel blockers on nerve impulses recorded from guinea-pig postganglionic sympathetic nerve terminals.

1. A focal extracellular suction electrode was used to investigate the contributions of K+ and Ca2+ currents to the nerve impulse recorded from sympathetic nerve terminals innervating the guinea-pig vas deferens in vitro. 2. Perfusing the electrode with Cd2+ (0.1-0.5 mM) had little effect on the configuration of the nerve impulse. 3. Perfusing the electrode with Ba2+ (1-3 mM) caused the appearance of a second negative-going component of the nerve impulse. Local application of Cd2+ (0.1 mM) had little affect on this component of the nerve impulse. 4. Perfusing the electrode with 4-aminopyridine (4-AP) and/or tetraethylammonium (TEA) caused the appearance of a second negative-going component of the nerve impulse. This component has been termed the late negative-going component (LNC). 5. The LNC produced by local application of 1 mM 4-AP and 10 mM TEA was not changed when the solution perfusing the electrode contained no added Ca2+, 10 mM Ca2+ or omega-conotoxin GVIA (0.1 microM). Perfusion of the electrode with Cd2+ (0.1 mM) reduced the amplitude and slowed the time course of the LNC. 6. The LNC was markedly inhibited when the organ bath was perfused with TEA (10 mM) or 4-AP and TEA (1 and 10 mM, respectively). In some experiments the LNC was completely abolished. 7. The LNC was reduced in amplitude and slowed in time course when the solution perfusing the organ bath contained no added Ca2+. A similar effect on the LNC was observed when the solution perfusing the organ bath contained omega-conotoxin GVIA (0.1 microM), charybdotoxin (0.05 microM) or low concentrations of TEA (0.3-1 mM) or Ba2+ (10-500 microM). 8. Bath application of the alpha 2-adrenoceptor agonist clonidine (0.1-0.3 microM) did not detectably change the LNC. 9. The results demonstrate that the LNC produced by the local application of K+ blockers is due primarily to K+ efflux from sites outside the recording electrode and that a part of the change in conductance that underlies this component is due to opening of Ca(2+)-activated K+ channels. The failure to detect an effect of clonidine on the LNC suggests that activation of presynaptic alpha 2-adrenoceptors does not change either the K+ or the Ca2+ conductance of the nerve terminals.

4-Aminopyridine↗
PubMed1985

Excitation-contraction coupling in crab muscle fibers with swollen T tubules.

Single crab (Callinectes danae) fibers were equilibrated with isotonic, high KCl solutions and were subsequently returned to the control saline. This caused marked swelling of the T tubules. Fibers treated with 100 mM KCl had a 2.5-mV residual depolarization, a 50% decrease in effective membrane resistance (Reff) and a 75% reduction in membrane time constant (tau m). These fibers exhibited large increases in membrane conductance upon depolarization and were inexcitable; membrane depolarization with current pulses elicited no contraction. The effects of the KCl treatment on membrane properties were not reproduced by treatment with high potassium gluconate solutions, which did not cause tubular swelling. Tetrabutylammonium (10 mM) or Ba ions (10-20 mM), but not tetraethylammonium (40-100 mM), Sr ions (15-70 mM), or procaine (1-8 mM) reversed the effects of the KCl treatment on Reff, tau m, membrane excitability, and excitation-contraction coupling. The time course of the Ba effects was consistent with the suggestion that the KCl treatment increases the K conductance of the tubular membranes, which in turn prevents the activation of voltage-dependent Ca channels located in the membranes of the T system. This results in inhibition of the Ca-dependent electrogenesis and consequently, the absence of contraction upon depolarization of the plasma membrane.

Animals↗
PubMed1991

Regulation of calcium-activated potassium efflux by neurotensin and other agents in HT-29 cells.

Neurotensin receptors have been shown previously to be coupled to polyphosphoinositide turnover and intracellular Ca2+ ([Ca2+]i) mobilization in HT-29 colonic epithelial cells (Bozou et al. Biochem. J. 264: 871, 1989; Turner et al. J. Pharmacol. Exp. Ther. 253: 1049, 1990). In this study, neurotensin was found to enhance dramatically the Ba2(+)- and tetraethylammonium chloride-sensitive K(+)-efflux rate (measured with 86Rb+) in the presence of ouabain and bumetanide, with basal efflux increasing 4.5 +/- 0.5-fold with 10 nM neurotensin. The K(+)-efflux rate, which was partially dependent on the extracellular Ca2+ concentration, was also increased by carbachol and ATP, two other [Ca2+]i-mobilizing agonists in HT-29 cells, as well as by the Ca2+ ionophores ionomycin and A23187, suggesting that the efflux was through Ca2(+)-activated K+ channels. Pretreatment of cells with neurotensin, carbachol, or ATP desensitized subsequent neurotensin-stimulated efflux by 82, 57, and 63%, respectively, confirming our previous results which indicated homologous and heterologous desensitization of the neurotensin receptor-signal transduction pathway. Pretreatment of cells with the protein kinase C activators phorbol 12-myristate 13-acetate (PMA) and mezerein did not affect [Ca2+]i mobilization or K+ efflux directly but desensitized neurotensin-stimulated efflux by greater than 80%. Pretreatment (2 h) with PMA also decreased K+ efflux in response to ionomycin by 59%, although ionomycin-induced [Ca2+]i mobilization was not inhibited. Downregulation of protein kinase C by overnight pretreatment with PMA resulted in recovery of ionomycin-stimulated efflux. These results suggest that agonist-stimulated Ca2(+)-activated K+ channels in HT-29 cells are regulated at multiple steps in the signal transduction pathway.

Adenocarcinoma↗