ArticleBritish journal of pharmacology1999
Dual actions of the metabolic inhibitor, sodium azide on K(ATP) channel currents in the rat CRI-G1 insulinoma cell line.
Article in British journal of pharmacology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 41 citations in OpenAlex.
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- Transformable nano-antibiotics for mechanotherapy and immune activation against drug-resistant Gram-negative bacteria.Science advances · 2023Article
- Microbial Fuel Cell-Based Biosensors and Applications.Applied biochemistry and biotechnology · 2023Review
- Nitrate leaching and its implication for Fe and As mobility in a Southeast Asian aquifer.FEMS microbiology ecology · 2023Article
- Visualizing cytoplasmic ATP inSTAR protocols · 2022Article
- Discrimination of Receptor-Mediated Endocytosis by Surface-Enhanced Raman Scattering.Langmuir : the ACS journal of surfaces and colloids · 2022Article
- Mitochondrial Inhibition by Sodium Azide Induces Assembly of eIF2α Phosphorylation-Independent Stress Granules in Mammalian Cells.International journal of molecular sciences · 2022Article
- Study of Uptake Mechanisms of Halloysite Nanotubes in Different Cell Lines.International journal of nanomedicine · 2021Article
- Microbial Fuel Cell-Based Biosensors.Biosensors · 2019Review
- Nrf2 Signaling in Sodium Azide-Treated Oligodendrocytes Restores Mitochondrial Functions.Journal of molecular neuroscience : MN · 2018Article
- A flow cytometry assay to quantify intercellular exchange of membrane components.Chemical science · 2017Article
- Riluzole But Not Melatonin Ameliorates Acute Motor Neuron Degeneration and Moderately Inhibits SOD1-Mediated Excitotoxicity Induced Disrupted Mitochondrial CaFrontiers in cellular neuroscience · 2016Article
- Sulfonylurea receptor 1 in central nervous system injury: a focused review.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2012Review
- Role of the amino-terminal transmembrane domain of sulfonylurea receptor SUR2B for coupling to K(IR)6.2, ligand binding, and oligomerization.Naunyn-Schmiedeberg's archives of pharmacology · 2012Article
- Role of adenosine A1 and A3 receptors in regulation of cardiomyocyte homeostasis after mitochondrial respiratory chain injury.American journal of physiology. Heart and circulatory physiology · 2005Article
- The aminoguanidine carboxylate BVT.12777 activates ATP-sensitive K+ channels in the rat insulinoma cell line, CRI-G1.BMC pharmacology · 2004Article
- Functional coupling between sulfonylurea receptor type 1 and a nonselective cation channel in reactive astrocytes from adult rat brain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2003Article
- Cell swelling and a nonselective cation channel regulated by internal Ca2+ and ATP in native reactive astrocytes from adult rat brain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2001Article
- Direct interaction of Na-azide with the KATP channel.British journal of pharmacology · 2000Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. The effects of various inhibitors of the mitochondrial electron transport chain on the activity of ATP-sensitive K+ channels were examined in the Cambridge rat insulinoma G1 (CRI-G1) cell line using a combination of whole cell and single channel recording techniques. 2. Whole cell current clamp recordings, with 5 mM ATP in the pipette, demonstrate that the mitochondrial uncoupler sodium azide (3 mM) rapidly hyperpolarizes CRI-G1 cells with a concomitant increase in K+ conductance. This is due to activation of K(ATP) channels as the sulphonylurea tolbutamide (100 microM) completely reversed the actions of azide. Other inhibitors of the mitochondrial electron transport chain, rotenone (10 microM) or oligomycin (2 microM) did not hyperpolarize CRI-G1 cells or increase K+ conductance. 3. In cell-attached recordings, bath application of 3 mM sodium azide (in the absence of glucose) resulted in a rapid increase in K(ATP) channel activity, an action readily reversible by tolbutamide (100 microM). Application of sodium azide (3 mM), in the presence of Mg-ATP, to the intracellular surface of excised inside-out patches also increased K(ATP) channel activity, in a reversible manner. 4. In contrast, rotenone (10 microM) or oligomycin (2 microM) did not increase K(ATP) channel activity in either cell-attached, in the absence of glucose, or inside-out membrane patch recordings. 5. Addition of sodium azide (3 mM) to the intracellular surface of inside-out membrane patches in the presence of Mg-free ATP or the non-hydrolysable analogue 5'-adenylylimidodiphosphate (AMP-PNP) inhibited, rather than increased, K(ATP) channel activity. 6. In conclusion, sodium azide, but not rotenone or oligomycin, directly activates K(ATP) channels in CRI-G1 insulin secreting cells. This action of azide is similar to that reported previously for diazoxide.
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