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At least 19 recordsLinked to original sources
PubMed1982

Block of outward current in cardiac Purkinje fibers by injection of quaternary ammonium ions.

We have studied the effects of iontophoretic injection of the quaternary ammonium compounds tetraethylammonium (TEA) and tetrabutylammonium (TBA) in cardiac purkinje fibers. We find that TBA(+) is a more effective blocker than TEA(+), but injection of either compound reduces the time-dependent outward plateau currents, transient outward current (I(to)), and the delayed rectifier (I(x)). Our findings provide evidence that these outward cardiac currents are carried by channels that in some respects are pharmacologically similar to squid axon potassium channels. We demonstrate that this procedure is a new tool that can be useful in the analysis of membrane currents in the heart.

Animals↗
PubMed1995

Muscarinic regulation of the cardiac CFTR Cl- current by quaternary ammonium compounds.

In guinea pig ventricle, the protein kinase A-regulated Cl- current (ICl) is conducted by an alternatively spliced isoform of the cystic fibrosis transmembrane conductance regulator. We studied muscarinic regulation of this current using the whole-cell configuration of the patch-clamp technique. Acetylcholine (ACh) antagonized activation of ICl activated by 1 microM isoproterenol (ISO) in a concentration-dependent manner. The concentration of ACh that produced a half-maximal effect (K1/2) was 36 nM, the slope factor was 1.1, and the relative magnitude of the Cl- conductance at maximally effective concentrations of ACh (Gmin) was 21% of that observed in the presence of ISO alone. In the presence of 100 nM atropine, a competitive antagonist at the muscarinic receptor, the K1/2 value for ACh inhibition of ICl was increased to 4.3 microM, but the slope factor and Gmin were not affected, which indicated that the dissociation constant (KB) for atropine was < 1 nM. ACh-induced inhibition of the ISO-activated ICl was also blocked by the quaternary ammonium compound tetraethylammonium (TEA). Like atropine, TEA increased the K1/2 value for ACh inhibition of ICl without affecting the slope factor or Gmin. Schild analysis confirmed that TEA is also a competitive antagonist at the muscarinic receptor, with a KB value of 137 microM. However, tetramethylammonium (TMA), a structurally related compound, acted as an agonist at the muscarinic receptor. TMA inhibited ICl activated by 1 microM ISO with a K1/2 value of 342 microM, a slope factor of 0.87 and a Gmin value of 17%. Increasing the concentration of ISO shifted the K1/2 value for both ACh and TMA inhibition of ICl to higher concentrations and increased Gmin, without significantly affecting the slope factor. These results indicate that muscarinic regulation of ICl depends on the level of beta adrenergic stimulation in a functionally uncompetitive manner. They also suggest that TMA acts like ACh, a full agonist at the muscarinic receptor. Furthermore, we conclude that quaternary ammonium compounds, which are often used as ion substitutes and direct ion channel blockers, should be used with caution because of the significant and diverse effects they exert at muscarinic receptors.

Acetylcholine↗
PubMed2003

The three-dimensional coordination polymer tetraethylammonium (ethylenediamine)cadmium(II) hexacyanoferrate(III), (Et(4)N)[[Cd(en)](4)[Fe(CN)(6)](3)].

The title compound, tetraethylammonium dodeca-mu-cyano-hexacyanotetrakis(ethylenediamine)tetracadmium(II)triferrate(III), (C(8)H(20)N)[Cd(4)Fe(3)(CN)(18)(C(2)H(8)N(2))(4)], was prepared from a reaction mixture containing CdCl(2), K(3)[Fe(CN)(6)], ethylenediamine (en) and [Et(4)N]Br in a 1:1:3:1 molar ratio. The crystal structure consists of a negatively charged three-dimensional framework of [[Cd(en)](4)[Fe(CN)(6)](3]n)(n-) anions, with [Et(4)N](+) cations located in the cavities of the framework. The Cd atom is octahedrally coordinated by one disordered chelating en molecule [mean Cd-N = 2.35 (3) A] and four N-bonded bridging cyano groups [Cd-N distances are in the range 2.283 (2)-2.441 (2) A]. There are two crystallographically independent [Fe(CN)(6)](3-) anions in the structure and in each the Fe atom lies on a twofold axis. In the first [mean Fe-C = 1.941 (5) A], all the cyano groups are bridging ligands, while in the second [mean Fe-C = 1.945 (2) A], there are two terminal cyano ligands in trans positions. The Cd-N-C angles range from 128.6 (2) to 172.8 (2) degrees.

Journal Article↗
PubMedDate not supplied

Binding of organic compounds to rat liver and lung.

The binding of various radioisotopically labeled organic compounds to rat liver and lung was investigated in vitro. Pieces of rat lung and slices of rat liver were incubated at 37 degrees C under a nitrogen atmosphere in a modified Krebs-Ringer phosphate solution (pH 7.4) CONTAININg the compound to be studied. Of the neutral compounds investigated, digitoxin, digoxin and dexamethasone were highly bound to both liver and lung tissue, whereas the degree of binding of amitrole, erythritol, and ouabain was 20% or less. The weak acids which were bound to the greatest extent in both liver and lung were phenobarbital, pentobarbital, and diphenylhydantoin. Barbital was poorly bound, and there was no evidence for the binding of 5,5-dimethyloxazolidine-2,4-dione or p-aminohippuric acid in either tissue. Binding of the cardiac glycosides and the barbiturates directly paralleled their lipid solubilities. The degree of binding of neutral compounds and weak acids to lung and liver tissue did not vary greatly with concentration, even though broad concentration ranges were studied. This was also true of the weak base morphine. On the other hand, the binding to liver and lung of the organic bases nicotine, pilocarpine, d-amphetamine, lidocaine, erythromycin, and chloroquine, did vary with concentration. The quaternary ammonium compound decamethonium was bound only to liver, and this binding also varied with concentration. Two additional quaternary ammonium compounds, tetraethylammonium and N1-methylnicotinamide, were not significantly bound to either tissue. Comparisons on the basis of equal content of solids revealed that the binding of diverse organic compounds in liver is greater than or equal to that in lung.

Amitrole↗
PubMed2000

Inhibition of aquaporin-1 water permeability by tetraethylammonium: involvement of the loop E pore region.

Previously, the only known blockers of water permeability through aquaporin-1 (AQP1) water channels were mercurial reagents such as HgCl(2). For AQP1, inhibition by mercury has been attributed to the formation of a mercaptide bond with cysteine residue 189 found in the putative pore-forming region loop E. Here we show that the nonmercurial compound, tetraethylammonium (TEA) chloride, reduces the water permeability of human AQP1 channels expressed in Xenopus oocytes. After preincubation of the oocytes for 15 min with 100 microM TEA, AQP1 water permeability was reduced by 20 to 40%, a degree of partial block similar to that obtained with 15 min of incubation in 100 microM HgCl(2). The reduction of water permeability was dose-dependent for tested concentrations up to 10 mM TEA. TEA blocks the Shaker potassium channel by interacting with a tyrosine residue in the outer pore region. We tested whether an analogous tyrosine residue in loop E of AQP1 could be involved in the binding of TEA. Using polymerase chain reaction, tyrosine 186 in AQP1, selected for its proximity to the mercury-binding site, was mutated to phenylalanine (Y186F), alanine (Y186A), or asparagine (Y186N). Oocyte expression of the mutant AQP1 channels showed that the water permeability of Y186F was equivalent to that of wild-type AQP1; the other mutant channels did not conduct water. However, in contrast to wild-type AQP1, the water permeability of Y186F was not reduced with 100 microM TEA. These results suggest that TEA reduces AQP1 water permeability by interacting with loop E.

Animals↗
PubMed1999

Probing of NMDA channels with fast blockers.

Using whole-cell patch-clamp techniques, we studied the interaction of open NMDA channels with tetraalkylammonium compounds: tetraethylammonium (TEA), tetrapropylammonium (TPA), tetrabutylammonium (TBA), and tetrapentylammonium (TPentA). Analysis of the blocking kinetics, concentration, and agonist dependencies using a set of kinetic models allowed us to create the criteria distinguishing the effects of these blockers on the channel closure, desensitization, and agonist dissociation. Thus, it was found that TPentA prohibited, TBA partly prevented, and TPA and TEA did not prevent either the channel closure or the agonist dissociation. TPentA and TBA prohibited, TPA slightly prevented, and TEA did not affect the channel desensitization. These data along with the voltage dependence of the stationary current inhibition led us to hypothesize that: (1) there are activation and desensitization gates in the NMDA channel; (2) these gates are distinct structures located in the external channel vestibule, the desensitization gate being located deeper than the activation gate. The size of the blocker plays a key role in its interaction with the NMDA channel gating machinery: small blockers (TEA and TPA) bind in the depth of the channel pore and permit the closure of both gates, whereas larger blockers (TBA) allow the closure of the activation gate but prohibit the closure of the desensitization gate; finally, the largest blockers (TPentA) prohibit the closure of both activation and desensitization gates. The mean diameter of the NMDA channel pore in the region of the activation gate localization was estimated to be approximately 11 A.

Animals↗
PubMedDate not supplied

[Regulation of the heat resistance of muscle fibers in Rana temporaria tadpoles by selecting the parental gametes using quaternary ammonium compounds and chelators].

In experiments on the frog Rana temporaria, studies have been made on the effect of selection of the parental sperm by quaternary ammonium compounds--tetraethylammonium and tetramethylammonium, as well as by chelating agents--EDTA and EGTA--on the heat resistance of muscle tissue in the progeny of the first generation. It was found that selection of the sperm for its maximum stability to the injurious (immobilizing) effect of these drugs affects quantitative relationship in the family between tadpoles with a high and low heat resistance of muscle fibers. Insemination of the eggs by the sperm with maximum stability to elimination by TEA and TMA favours the development of tadpoles with relatively low heat resistance of muscle fibers. On the contrary, sperm selection by EDTA and EDTA increases the amount of tadpoles with a higher heat resistance of muscles.

Animals↗
PubMed1995

Quaternary ammonium ion blockade of IK in nerve axons revisited. Open channel block vs. state independent block.

The mechanism of blockade of the delayed rectifier potassium ion channel in squid giant axons by intracellular quaternary ammonium ions (QA) appears to be remarkably sensitive to the structure of the blocker. TEA, propyltriethyl-ammonium (C3), and propyltetraethylammonium (TAA-C3) all fail to alter the deactivation, or "tail" current time course following membrane depolarization, even with relatively large concentrations of the blockers, whereas butyltriethylammonium (C4), butyltetraethylammonium (TAA-C4), and pentytriethyammonium (C5) clearly do have such an effect. The relative electrical distance of blockade for all of these ions is approximately 0.25-0.3 from the inner surface of the membrane. The observations concerning TEA, C3, and TAA-C3 suggest that these ions can block the channel in either its open or its closed state. The results with C4, TAA-C4, and C5 are consistent with the open channel block model. Moreover, the sensitivity of block mechanism to the structure of the blocker suggests that the gate is located close to the QA ion binding site and that TEA, C3, and TAA-C3 do not interfere with channel gating, whereas C4, TAA-C4, C5, and ions having a longer hydrophobic "tail" than C5 do have such an effect. The parameters of block obtained for all QA ions investigated were unaffected by changes in the extracellular potassium ion concentration.

Animals↗
PubMed1995

The effect of crown ethers, tetraalkylammonium salts, and polyoxyethylene amphiphiles on pirarubicin incorporation in K562 resistant cells.

The basic distinguishing feature of all cells expressing functional P-glycoprotein-multidrug resistance (P-gp-MDR) is a decrease in steady-state accumulation drug levels as compared to drug-sensitive controls. In an attempt to identify mechanism(s) by which MDR can be circumvented, we examined the cellular accumulation, in resistant cells, of 4'-O-tetrahydropyranyl-doxorubicin (pirarubicin) alone and in conjunction with various molecules belonging to three different classes: the crown ethers, the tetraalkylammonium salts, and the polyoxethylene amphiphiles. The present study was performed using a spectrofluorometric method which enabled us to follow the uptake and release of fluorescent molecules by living cells while the cells were being incubated with the drug. Erythroleukemia K562 cell lines were used. Our data show that the compounds of these three completely different classes were able to increase the incorporation of pirarubicin provided they had a minimum degree of lipophilicity. Study of the growth inhibitory activity of these compounds revealed that cross-resistance to the tetraalkyl ammonium salt increased with the lipophilicity and was equal to 58 for tetraoctylammonium salt, the most lipophilic compound of this series. This demonstrates that neither the presence of a positive charge nor an aromatic moiety is required for MDR recognition.

Antibiotics, Antineoplastic↗
PubMed1986

The effect of depletion of nonprotein sulfhydryls by diethyl maleate plus buthionine sulfoximine on renal uptake of mercury in the rat.

Rats pretreated with diethyl maleate (DEM, 3.37 mmol/kg, ip) and buthionine sulfoximine (BSO, 0.45 mmol/kg, ip) and subsequently given mercuric chloride (HgCl2, 0.014 mmol/kg, sc) had a significantly greater mortality rate over the 24 hr after injection than rats given only HgCl2 or HgCl2 following either DEM or BSO alone. Depletion of nonprotein sulfhydryls (NPSH) in the kidney significantly decreased mercury uptake in that organ. A similar effect was not seen in the liver despite marked depletion of NPSH. Similarly, there was a tendency for less in vitro mercury accumulation in renal cortical slices from rats made glutathione deficient by DEM + BSO compared to control, or rats made glutathione deficient by DEM or BSO alone. Depletion of nonprotein sulfhydryls by the combination of the depleting agents diethyl maleate plus buthionine sulfoximine (DEM + BSO) had a greater effect to alter organic ion accumulation in renal cortical slices than the agents alone. The higher mortality produced by mercuric chloride after DEM + BSO pretreatment may have been due to an increased availability of mercury in lethal concentrations at other organ sites. These data suggest the possible importance of NPSH in renal mercuric ion accumulation, but not in the liver.

Animals↗