Disease relevance of tetraethylammonium

• In the case of K(+) antagonists used in animal research, 4-aminopyridine blocked E. coli chemotaxis between 10(-3) M and, totally, 10(-2) M, while motility was not affected at 10(-2) M; on the other hand, tetraethylammonium chloride failed to inhibit either chemotaxis or motility at 10(-2) M [1].
• In vitro reversal of cardiac deterioration in septic shock with tetraethylammonium chloride [2].
• Tetraethylammonium chloride or other drugs that decrease outward potassium current and prolong the action potential duration may be helpful in treating cardiac dysfunction that accompanies sepsis [2].
• This was confirmed by showing that inhibition of the K+ channel opening by tetraethylammonium chloride can reverse the effect of BaP on oxytocin-induced Ca2+ oscillations, and potentially decrease the toxicity of BaP [3].

High impact information on tetraethylammonium

• The heteromultimeric RCK1, 4 channel mediates a transient potassium outward current, similar to the RCK4 channel but inactivates more slowly, has a larger conductance and is more sensitive to block by dendrotoxin and tetraethylammonium chloride [4].
• The use of a potassium-blocking agent to prolong action potentials may seem surprising because we previously found tetraethylammonium chloride (TEA), another potassium blocker, ineffective on normal rat myelinated fibres, and two recent voltage-clamp studies have confirmed that mammalian nodes have few, if any, potassium channels [5].
• Under conditions that eliminate the base composition effect on thermal stability (2.4 M tetraethylammonium chloride), such an anlysis can distinquish "thermal classes" of repetitive DNA duplexes exhibiting different amounts of base pair mismatch [6].
• Canine cardiac Purkinje fibers exposed to sodium-free solutions containing 16 mM CaCl2, 20 mM tetraethylammonium chloride, 108 mM tetramethylammonium chloride, and 2.7 mM KCl may be quiescent at a resting potential of either -50 mV or -90 mV [7].
• To investigate this, we have recorded intracellularly in slices of rat neocortex bathed in 24 mM tetraethylammonium chloride and 1 microM TTX [8].

Biological context of tetraethylammonium

• To determine whether these assemblies were functional we created rSK3VF, an rSK3 mutant with an enhanced affinity for tetraethylammonium chloride (TEA) (IC50 of 0.3 mM) [9].
• However, vasodilation caused by the 2 lower doses of BK were significantly attenuated after K(Ca) channel activity was blocked with tetraethylammonium chloride (0.1 mg. 100 mL FAV(-1). min(-1)), suggesting that in the lower dose range, BK mediates vasodilation through the opening of vascular potassium channels [10].
• On the basis of its kinetics, a reversal potential of -85 +/- 6 mV (n = 6), sensitivity to intracellularly injected tetraethylammonium chloride (TEA), and its slow and partial inactivation (approximately 25%) this mechanism is classified as a delayed rectifier potassium conductance [11].
• The thermal stability of interspecies DNA duplexes was measured in a solvent (2.4 M tetraethylammonium chloride) that suppresses the effect of base composition on melting temperature [12].
• Tetraethylammonium chloride (TEA), a blocker of the calcium (Ca2+)-dependent K+ conductances of GH3, was found to reversibly inhibit cell proliferation, as measured by 3H-thymidine incorporation [13].

Anatomical context of tetraethylammonium

• However, to visualize the postsynaptic smooth muscle response, it was necessary to treat the isolated preparation with tetraethylammonium chloride (TEA) [14].
• Early effects of tetraethylammonium chloride on the contractile properties of isolated rabbit basilar arteries [15].
• Tetraethylammonium chloride induced greater contractions in control aortas compared with aortas from pregnant rats [16].
• The effect of tetraethylammonium chloride on calcium fluxes in smooth muscle from rabbit main pulmonary artery [17].
• The effect of tetraethylammonium chloride on potassium permeability in the smooth muscle cell membrane of canine trachea [18].

Associations of tetraethylammonium with other chemical compounds

• Exocytosis of PMN granule contents was blocked with 80 mM tetraethylammonium chloride, 2 mM dibutyryl cyclic adenosine monophosphate, or 2 mM magnesium ethylene glycol-bis(beta-aminoethyl ether)-N,N-tetraacetate in calcium-free medium [19].
• Nicotinic blocking agents, hexamethonium, tetraethylammonium chloride, and trimethaphan, blocked VP release in response to the addition of sufficient NaCl to yield a 10 mosm/kg H2O increase in culture medium osmolality [20].
• Inhibition of the ACh-induced extracurrent on atrial fibres of Rana esculenta by atropine and tetraethylammonium chloride [proceedings] [21].
• 4. The second, slow type of IPSP has a long rise time (1-2 s), is mediated by increased conductance to potassium (with little or no involvement of chloride), and is not blocked by 10 microM PTX, 5 mM tetraethylammonium chloride, or 0.1 mM scopolamine [22].
• With endothelium intact, N(omega)-nitro-l-arginine (l-NNA), 1H-[1,2,4]oxadiazolo-[4,3-a]quinoxalin-1-one (ODQ), or tetraethylammonium chloride (TEA(+)), inhibitors of NO synthase (NOS), guanylyl cyclase, and large-conductance Ca(2+)-activated K(+) (K(Ca)) channels, respectively, also blocked dilation induced by DMDC [23].

Gene context of tetraethylammonium

• Maximum relaxation response to CRP (79.5+/-10%) was attenuated by KCl (2.5+/-11.5%, P<0.001), BaCl (24.5+/-7.5%, P<0.001), and tetraethylammonium chloride (34.9+/-8.25%, P<0.01) but not by glibenclamide [24].
• PACAP provoked a sustained increase of the resting membrane potential in cerebellar granule cells cultured either in high or low KCl-containing medium, and this long-term depolarizing effect of PACAP was mimicked by the I(K) specific blocker tetraethylammonium chloride (TEA) [25].
• The HGF-induced K+ current was abolished when tetraethylammonium chloride was added in bathing solution or a low Ca2+ solution was included in the recording pipette [26].
• Intravenous injection of tetraethylammonium chloride (TEA) into rats on the 8.0% NaCl diet decreased the activities of p38 MAP kinase and p42/44 MAP kinase, compared with rats on the same diet and given vehicle intravenously [27].
• The outward K+ current can be inhibited by tetraethylammonium chloride (TEA) whereas the Cl- current is inhibited by the Cl- channel blockers 5-nitro-2-(3-phenylpropylamino) (NPPB) and N-phenylanthranilic acid (DPC) [28].

Analytical, diagnostic and therapeutic context of tetraethylammonium

• 1. Conventional microelectrodes, the Na+ channel blocker amiloride (0.1 mM), and the K+ channel blocker tetraethylammonium chloride (TEA, 30 mM) were used to examine the effects of corticosteroid hormones administered in vivo on the Na+ and K+ transport properties of isolated rat distal colon [29].
• External application of tetraethylammonium chloride caused membrane depolarization (10-15 mV), spontaneous discharge of action potentials and rhythmic arteriolar constriction [30].
• 1. Retzius cells of leech segmental ganglia were exposed to tetraethylammonium chloride (TEA) presented both extracellularly, dissolved in the perfusing fluid, and intracellulary, by iontophoresis from a microelectrode [31].
• The spike with an overshoot evoked by electrical stimulation in the presence of tetraethylammonium chloride (TEA) was suppressed by 2-NN, mainly due to hyperpolarization of the membrane and not to suppression of Ca-carriers at the membrane [32].
• This inhibitory response was not blocked by bilateral vagotomy, spinal transection, splanchnectomy, or the intravenous administration of tetraethylammonium chloride [33].

References