ArticleBritish journal of pharmacology2003
The Cl(-) channel blocker niflumic acid releases Ca(2+) from an intracellular store in rat pulmonary artery smooth muscle cells.
Article in British journal of pharmacology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 46 citations in OpenAlex.
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- ANO1 channels are expressed in mouse urethral smooth muscle but do not contribute to agonist or neurally evoked contractions.Scientific reports · 2025Article
- Mapping the rat gastric slow-wave conduction pathway: bridging in vitro and in vivo methods, revealing a loosely coupled region in the distal stomach.American journal of physiology. Gastrointestinal and liver physiology · 2024Article
- ML277 specifically enhances the fully activated open state of KCNQ1 by modulating VSD-pore coupling.eLife · 2019Article
- Effects of new-generation TMEM16A inhibitors on calcium-activated chloride currents in rabbit urethral interstitial cells of Cajal.Pflugers Archiv : European journal of physiology · 2017Article
- Flavones modulate respiratory epithelial innate immunity: Anti-inflammatory effects and activation of the T2R14 receptor.The Journal of biological chemistry · 2017Article
- Cyclic-nucleotide-gated cation current and Ca2+-activated Cl current elicited by odorant in vertebrate olfactory receptor neurons.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- NSAIDs modulate GABA-activated currents via CaExperimental and therapeutic medicine · 2016Article
- Molecular and functional significance of Ca(2+)-activated Cl(-) channels in pulmonary arterial smooth muscle.Pulmonary circulation · 2015Review
- The transmembrane protein 16A Ca(2+)-activated Cl- channel in airway smooth muscle contributes to airway hyperresponsiveness.American journal of respiratory and critical care medicine · 2013Article
- Novel 5-substituted benzyloxy-2-arylbenzofuran-3-carboxylic acids as calcium activated chloride channel inhibitors.Bioorganic & medicinal chemistry · 2012Article
- A Ca²⁺-dependent chloride current and Ca²⁺ influx via Ca(v)1.2 ion channels play major roles in P2Y receptor-mediated pulmonary vasoconstriction.British journal of pharmacology · 2012Article
- Mechanisms of U46619-induced contraction of rat pulmonary arteries in the presence and absence of the endothelium.British journal of pharmacology · 2009Article
- Caffeine-inducible ATP release is mediated by Ca2+-signal transducing system from the endoplasmic reticulum to mitochondria.Naunyn-Schmiedeberg's archives of pharmacology · 2008Article
- Niflumic acid inhibits chloride conductance of rat skeletal muscle by directly inhibiting the CLC-1 channel and by increasing intracellular calcium.British journal of pharmacology · 2007Article
- CaMKII inactivation by extracellular Ca(2+) depletion in dorsal root ganglion neurons.Cell calcium · 2006Article
- Distribution of cGMP-dependent and cGMP-independent Ca(2+)-activated Cl(-) conductances in smooth muscle cells from different vascular beds and colon.Pflugers Archiv : European journal of physiology · 2005Article
- Escherichia coli heat stable (STa) enterotoxin and the upper small intestine: lack of evidence in vivo for net fluid secretion.The Journal of membrane biology · 2005Article
- The Cl(-) channel blocker niflumic acid releases Ca(2+) from an intracellular store in rat pulmonary artery smooth muscle cells.British journal of pharmacology · 2003Article
- Modeling of the role of Cl- channels in Ca2+ translocation through endoplasmic reticulum membrane.Doklady. Biochemistry and biophysicsArticle
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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
The effect of the Cl- channel blockers niflumic acid (NFA), 5-nitro-2-(3-phenylpropylamino)-benzoic acid (NPPB), 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS), and anthracene-9-carboxylic acid (A-9-C), on Ca2+ signalling in rat pulmonary artery smooth muscle cells was examined. Intracellular Ca2+ concentration ([Ca2+]i) was monitored with either fura-2 or fluo-4, and caffeine was used to activate the ryanodine receptor, thereby releasing Ca2+ from the sarcoplasmic reticulum (SR). NFA and NPPB significantly increased basal [Ca2+]i and attenuated the caffeine-induced increase in [Ca2+]i. These Cl- channel blockers also increased the half-time (t1/2) to peak for the caffeine-induced [Ca2+]i transient, and slowed the removal of Ca2+ from the cytosol following application of caffeine. Since DIDS and A-9-C were found to adversely affect fura-2 fluorescence, fluo-4 was used to monitor intracellular Ca2+ in studies involving these Cl- channel blockers. Both DIDS and A-9-C increased basal fluo-4 fluorescence, indicating an increase in intracellular Ca2+, and while DIDS had no significant effect on the t1/2 to peak for the caffeine-induced Ca2+ transient, it was significantly increased by A-9-C. In the absence of extracellular Ca2+, NFA significantly increased basal [Ca2+]i, suggesting that the release of Ca2+ from an intracellular store was responsible for the observed effect. Depleting the SR with the combination of caffeine and cyclopiazonic acid prevented the increase in basal [Ca2+]i induced by NFA. Additionally, incubating the cells with ryanodine also prevented the increase in basal [Ca2+]i induced by NFA. These data show that Cl- channel blockers have marked effects on Ca2+ signalling in pulmonary artery smooth muscle cells. Furthermore, examination of the NFA-induced increase in [Ca2+]i indicates that it is likely due to Ca2+ release from an intracellular store, most probably the SR.
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