calcimycin and cetiedil

calcimycin has been researched along with cetiedil* in 7 studies

Other Studies

7 other study(ies) available for calcimycin and cetiedil

ArticleYear
Differences in the actions of some blockers of the calcium-activated potassium permeability in mammalian red cells.
    British journal of pharmacology, 1999, Volume: 126, Issue:1

    1. The actions of some inhibitors of the Ca2+-activated K+ permeability in mammalian red cells have been compared. 2. Block of the permeability was assessed from the reduction in the net loss of K+ that followed the application of the Ca2+ ionophore A23187 (2 microM) to rabbit red cells suspended at a haematocrit of 1% in a low potassium solution ([K]0 0.12-0.17 mM) at 37 degrees C. Net movement of K+ was measured using a K+-sensitive electrode placed in the suspension. 3. The concentrations (microM +/- s.d.) of the compounds tested causing 50% inhibition of K+ loss were: quinine, 37 +/- 3; cetiedil, 26 +/- 1; the cetiedil congeners UCL 1269, UCL 1274 and UCL 1495, approximately 150, 8.2 +/- 0.1, 0.92 +/- 0.03 respectively; clotrimazole, 1.2 +/- 0.1; nitrendipine, 3.6 +/- 0.5 and charybdotoxin, 0.015 +/- 0.002. 4. The characteristics of the block suggested that compounds could be placed in two groups. For one set (quinine, cetiedil, and the UCL congeners), the concentration-inhibition curves were steeper (Hill coefficient, nH, > or = 2.7) than for the other (clotrimazole, nitrendipine, charybdotoxin) for which nH approximately 1. 5. Compounds in the first set alone became less active on raising the concentration of K+ in the external solution to 5.4 mM. 6. The rate of K+ loss induced by A23187 slowed in the presence of high concentrations of cetiedil and its analogues, suggesting a use-dependent component to the inhibitory action. This was not seen with clotrimazole. 7. The blocking action of the cetiedil analogue UCL 1274 could not be overcome by an increase in external Ca2+ and its potency was unaltered when K+ loss was induced by the application of Pb2+ (10 microM) rather than by A23187. 8. These results, taken with the findings of others, suggest that agents that block the red cell Ca2+-activated K+ permeability can be placed in two groups with different mechanisms of action. The differences can be explained by supposing that clotrimazole and charybdotoxin act at the outer face of the channel whereas cetiedil and its congeners may block within it, either at or near the K+ binding site that determines the flow of K+.

    Topics: Analgesics, Non-Narcotic; Animals; Antisickling Agents; Azepines; Calcimycin; Calcium; Calcium Channel Blockers; Cell Membrane Permeability; Charybdotoxin; Clotrimazole; Dose-Response Relationship, Drug; Erythrocyte Membrane; Erythrocytes; Growth Inhibitors; Ionophores; Lead; Mammals; Nitrendipine; Potassium; Potassium Channel Blockers; Quinine; Rabbits; Time Factors

1999
Cyclosporin A affects functions concerning acetylcholine release of cholinergic Torpedo synaptosomes.
    European journal of pharmacology, 1996, Feb-05, Volume: 296, Issue:3

    The effect of cyclosporin A was investigated on Torpedo synaptosomes. Cyclosporin A inhibits KCl-evoked acetylcholine release (up to 50% at 1 mu M) and was inactive on acetylcholine release induced by a Ca2+ ionophore, A23187. Interestingly, when the synaptosomes were pretreated with cyclosporin A, this immunosuppressor did abolish the modulation of A23187-induced acetylcholine release produced by two other drugs, cetiedil (alpha-cyclohexyl-3-thienyl acetic acid 2-(hexahydro-1H-azepin-1-yl) ethyl ester, citrate salt) and MR16728 (N-(N'-hexamethylene imino)-propyl-phenyl-cyclohexyl-methyl acetamide, chlorhydrate), which were previously shown to be inhibitory and stimulatory, respectively. Moreover, cyclosporin A and MR16728 are competitive inhibitors of [3H]cetiedil binding to purified synaptosomal presynaptic membranes (dissociation constant of 181.9 nM). These results suggest that presynaptic proteins involved in acetylcholine release (directly or indirectly through cyclophilin) are potential targets of cyclosporin A in Torpedo synaptosomes.

    Topics: Acetamides; Acetanilides; Acetylcholine; Animals; Azepines; Calcimycin; Calcium; Cyclosporine; Immunosuppressive Agents; Potassium Chloride; Synaptosomes; Torpedo

1996
Spontaneous release of acetylcholine from Torpedo synaptosomes: effect of cetiedil and its analogue MR 16728.
    Journal of neurochemistry, 1994, Volume: 62, Issue:1

    The effects of cetiedil and its analogue MR 16728 were examined on spontaneous acetylcholine release measured with a chemiluminescent assay using choline oxidase in a synaptosomal suspension obtained from Torpedo marmorata electric organ. Evoked acetylcholine release is inhibited by cetiedil, whereas this drug enhances spontaneous extracellular Ca(2+)-independent acetylcholine release (up to 340%). This effect was examined as a function of cetiedil concentration and incubation time. On the other hand, the analogue MR 16728, which enhances A23187-evoked acetylcholine release, also enhances spontaneous Ca(2+)-independent acetylcholine release. Cetiedil and MR 16728 effects on spontaneous acetylcholine release were also examined in the presence of Ca2+. Addition of Ca2+ enhanced spontaneous acetylcholine release by 75%, and cetiedil and MR 16728 stimulation was maintained but with different levels of enhancement. Thus, these results show that the processes responsible for evoked and spontaneous acetylcholine release are sensitive but in different ways to drugs of the cetiedil family.

    Topics: Acetamides; Acetanilides; Acetylcholine; Animals; Anti-Arrhythmia Agents; Azepines; Calcimycin; Calcium; Electric Organ; Kinetics; Parasympathomimetics; Synaptosomes; Time Factors; Torpedo

1994
Mediatophore: a nerve terminal membrane protein supporting the final step of the acetylcholine release process.
    Progress in brain research, 1990, Volume: 84

    Topics: Acetylcholine; Animals; Azepines; Calcimycin; Calcium; Electric Organ; Liposomes; Membrane Proteins; Microscopy, Electron; Nerve Endings; Nerve Tissue Proteins; Proteolipids; Synaptosomes; Torpedo

1990
Compared effects of two vesicular acetylcholine uptake blockers, AH5183 and cetiedil, on cholinergic functions in Torpedo synaptosomes: acetylcholine synthesis, choline transport, vesicular uptake, and evoked acetylcholine release.
    Journal of neurochemistry, 1989, Volume: 52, Issue:3

    We examined the effects of two drugs, AH5183 and cetiedil, demonstrated to be potent inhibitors of acetylcholine (ACh) transport by isolated synaptic vesicles on cholinergic functions in Torpedo synaptosomes. AH5183 exhibited a high specificity toward vesicular ACh transport, whereas cetiedil was shown to inhibit both high-affinity choline uptake and vesicular ACh transport. Choline acetyltransferase was not affected by either drug. High external choline concentrations permitted us to overcome cetiedil inhibition of high-affinity choline transport, and thus synthesis of [14C]ACh in treated preparations was similar to that in controls. We then tested evoked ACh release in drug-treated synaptosomes under conditions where ACh translocation into the vesicles was blocked. We observed that ACh release was impaired only in cetiedil-treated preparations; synaptosomes treated with AH5183 behaved like the controls. Thus, this comparative study on isolated nerve endings allowed us to dissociate two steps in drug action: upstream, where both AH5183 and cetiedil are efficient blockers of the vesicular ACh translocation, and downstream, where only cetiedil is able to block the ACh release process.

    Topics: Acetylcholine; Animals; Azepines; Biological Transport; Calcimycin; Choline; Electric Organ; Hydrogen-Ion Concentration; Kinetics; Neuromuscular Depolarizing Agents; Phencyclidine; Piperidines; Synaptic Vesicles; Synaptosomes; Torpedo

1989
Effect of cetiedil on acetylcholine release and intramembrane particles in cholinergic synaptosomes.
    Biology of the cell, 1987, Volume: 61, Issue:1-2

    The release of acetylcholine (ACh) from instantly frozen Torpedo electric organ synaptosomes in the course of stimulation is systematically associated with an increase in the number of large intramembrane particles counted on freeze-fracture replicas. The drug cetiedil, which is a potent inhibitor of ACh release, also blocks the increase in the number of large particles. The blockage was studied either after ionophore A 23187 or Glycera neurotoxin action in the presence of calcium.

    Topics: Acetylcholine; Animals; Azepines; Calcimycin; Cell Membrane; Cholinergic Fibers; Electric Organ; Freeze Fracturing; Neurotoxins; Synaptosomes; Torpedo

1987
Oxpentifylline and cetiedil citrate improve deformability of dehydrated sickle cells.
    Journal of clinical pathology, 1987, Volume: 40, Issue:10

    Erythrocytes from 14 patients with homozygous sickle cell anaemia were treated with the calcium ionophore A23187 to induce loss of cellular potassium and water. The dehydrated cells showed a decrease in filterability (loss of deformability) through pores of 5 micron diameter. Oxpentifylline and cetiedil citrate, which preserve erythrocyte cation and water content, had a significant (p less than 0.01) protective effect against loss of deformability at a concentration of 1 mumol/l. Oxpentifylline showed no adverse effect on the rheology, morphology, or haemolysis of sickle cells at concentrations up to 500 mumol/l. Drugs that act on the erythrocyte membrane to maintain cell hydration are of potential rheological benefit in sickle cell anaemia.

    Topics: Anemia, Sickle Cell; Antisickling Agents; Azepines; Calcimycin; Dose-Response Relationship, Drug; Erythrocyte Deformability; Erythrocytes, Abnormal; Humans; Pentoxifylline; Theobromine

1987