ArticleBritish journal of pharmacology1994
Permeation properties and modulation of volume-activated Cl(-)-currents in human endothelial cells.
Article in British journal of pharmacology, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 68 citations in OpenAlex.
- Recent advances in the structure, function and regulation of the volume-regulated anion channels and their role in immunity.The Journal of physiology · 2025Review
- Physiology of the volume-sensitive/regulatory anion channel VSOR/VRAC. Part 1: from its discovery and phenotype characterization to the molecular entity identification.The journal of physiological sciences : JPS · 2024Review
- Vasodilators activate the anion channel TMEM16A in endothelial cells to reduce blood pressure.Science signaling · 2023Article
- Inhibiting Hv1 channel in peripheral sensory neurons attenuates chronic inflammatory pain and opioid side effects.Cell research · 2022Article
- Glia as a key factor in cell volume regulation processes of the central nervous system.Frontiers in cellular neuroscience · 2022Review
- Cell Volume Control in Healthy Brain and Neuropathologies.Current topics in membranes · 2018Review
- ATP release via anion channels.Purinergic signalling · 2005Article
- Volume-regulated anion channels serve as an auto/paracrine nucleotide release pathway in aortic endothelial cells.The Journal of general physiology · 2002Article
- Receptor-mediated control of regulatory volume decrease (RVD) and apoptotic volume decrease (AVD).The Journal of physiology · 2001Review
- Inhibition of volume-regulated anion channels in cultured endothelial cells by the anti-oestrogens clomiphene and nafoxidine.British journal of pharmacology · 2001Article
- Blockers of VacA provide insights into the structure of the pore.Biophysical journal · 2000Article
- Block by fluoxetine of volume-regulated anion channels.British journal of pharmacology · 1999Article
- Regulation of a swelling-activated chloride current in bovine endothelium by protein tyrosine phosphorylation and G proteins.The Journal of physiology · 1998Article
- Activation of volume-regulated chloride currents by reduction of intracellular ionic strength in bovine endothelial cells.The Journal of physiology · 1998Article
- A swelling-activated chloride current in rat sympathetic neurones.The Journal of physiology · 1997Article
- Calcium-activated chloride channels in bovine pulmonary artery endothelial cells.The Journal of physiology · 1997Article
- Membrane currents and the resting membrane potential in cultured bovine pulmonary artery endothelial cells.The Journal of physiology · 1996Article
- Cell swelling activates ATP-dependent voltage-gated chloride channels in M-1 mouse cortical collecting duct cells.The Journal of general physiology · 1996Article
- Potent block of volume-activated chloride currents in endothelial cells by the uncharged form of quinine and quinidine.British journal of pharmacology · 1996Article
- The volume-activated chloride current in endothelial cells from bovine pulmonary artery is not modulated by phosphorylation.Pflugers Archiv : European journal of physiology · 1996Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. We have studied the permeation and pharmacological properties of a recently described volume-activated, calcium-insensitive, small-conductance Cl(-)-channel in endothelial cells from human umbilical vein. 2. The relative permeability for various anions was I- > Cl- approximately Br- > F- > gluconate- (1.63 +/- 0.36: 1:0.95 +/- 0.16:0.46 +/- 0.04:0.19 +/- 0.07, n = 10). 3. 5-Nitro-2-(3-phenylpropylamino)-benzoic acid (NPPB) induced a fast and reversible block of the current (Ki = 29 mumol l-1). 4. Extracellular ATP induced a low-affinity block of the current, that showed a small voltage-dependence (K1 = 4.9 mmol l-1 at +80 mV and K1 = 8.2 mmol l-1 at -80 mV). 5. Extracellularly applied arachidonic acid (10 mumol l-1) irreversibly blocked the current in 5 out of 9 cells. This block seems to be non-specific, because other ionic currents, e.g. inwardly rectifying K+ currents, were blocked as well. 6. Tamoxifen induced a high affinity block of the current (K1 = 2.9 mumol l-1). Block and reversal of block were however much slower than with NPPB. 7. Cytotoxic compounds, which are substrates of the P-glycoprotein multidrug transporter, loaded into endothelial cells via the patch pipette, exerted only minor effects on the volume-activated current. Vinblastine and colcemid did not affect the volume-activated current, whereas daunomycin and vincristine induced a slow 'run-down' of the current. 8. The similarity between permeation and pharmacological properties of volume-activated Cl--currents in endothelial cells and those in many other cell types may suggest that they all belong to the same family of volume-activated small-conductance Cl--channels. Evidence that they belong to the class of P-glycoprotein associated Cl--channels is however only marginal, whereas their biophysical characteristics differ significantly from those of the CIC-2 volume-activated Cl--channels.
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