ArticleBritish journal of pharmacology2003
Anomalous effect of anthracene-9-carboxylic acid on calcium-activated chloride currents in rabbit 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 13 papers.
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Who cites it
13 citing papers in PubMed, 29 citations in OpenAlex.
- Function and Regulation of the Calcium-Activated Chloride Channel Anoctamin 1 (TMEM16A).Handbook of experimental pharmacology · 2024Article
- TMEM16A is implicated in the regulation of coronary flow and is altered in hypertension.British journal of pharmacology · 2019Article
- Drug Repurposing: The Anthelmintics Niclosamide and Nitazoxanide Are Potent TMEM16A Antagonists That Fully Bronchodilate Airways.Frontiers in pharmacology · 2019Article
- Extracellular protons enable activation of the calcium-dependent chloride channel TMEM16A.The Journal of physiology · 2017Article
- Influence of intracellular Ca2+ and alternative splicing on the pharmacological profile of ANO1 channels.American journal of physiology. Cell physiology · 2016Article
- Mechanism of allosteric activation of TMEM16A/ANO1 channels by a commonly used chloride channel blocker.British journal of pharmacology · 2016Article
- Molecular and functional significance of Ca(2+)-activated Cl(-) channels in pulmonary arterial smooth muscle.Pulmonary circulation · 2015Review
- Conditional knockout of TMEM16A/anoctamin1 abolishes the calcium-activated chloride current in mouse vomeronasal sensory neurons.The Journal of general physiology · 2015Article
- Pharmacological properties of native CaCCs and TMEM16A.Channels (Austin, Tex.) · 2014Article
- Pharmacological characterization of TMEM16A currents.Channels (Austin, Tex.) · 2014Article
- Cholesterol depletion alters amplitude and pharmacology of vascular calcium-activated chloride channels.Cardiovascular research · 2010Article
- Inhibition of vascular calcium-gated chloride currents by blockers of KCa1.1, but not by modulators of KCa2.1 or KCa2.3 channels.British journal of pharmacology · 2009Article
- Mechanism of the inhibition of Ca2+-activated Cl- currents by phosphorylation in pulmonary arterial smooth muscle cells.The Journal of general physiology · 2006Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1 Ca(2+)-activated Cl(-) currents (I(Cl(Ca))) evoked by K(+)-free pipette solutions containing 500 nM Ca(2+) were recorded in rabbit pulmonary artery smooth muscle cells. A voltage step protocol in which the cells were stepped to +70 mV and then to -80 mV produced outward and inward Cl(-) currents respectively that exhibited distinctive voltage- and time-dependent kinetics that remained consistent for the recording period. 2 Application of the Cl(-) channel inhibitor anthracene-9-carboxylic acid (A-9-C, 500 micro M), produced a small inhibition of the maximum outward Cl(-) current at +70 mV (21+/-10%) but augmented the amplitude of the instantaneous inward relaxation at -80 mV by 321+/-34% (n=12). 3 The current recorded in the absence and presence of A-9-C reversed at the theoretical Cl(-) equilibrium potential and the reversal potential was shifted by about -40 mV upon replacement of external chloride ion by the more permeant anion thiocyanate. Currents in the absence and presence of A-9-C were similarly affected by 100 micro M niflumic acid. 4 Augmentation of the inward current at -80 mV by A-9-C required prior depolarization, i.e. A-9-C did not simply activate a Cl(-) current at negative membrane potentials. Moreover the degree of augmentation was independent of the internal Ca(2+) for concentrations between 100 nM and 1 micro M Ca(2+). 5 The data from the present study confirm previous observations that the inhibitory effect of Cl(-) channel blockers is modified when [Ca(2+)](i) is maintained at higher than normal resting concentrations.
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