ArticleThe Journal of physiology1997
Contrasting effects of intracellular redox couples on the regulation of maxi-K channels in isolated myocytes from rabbit pulmonary artery.
Article in The Journal of physiology, 1997. 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, 45 citations in OpenAlex.
- Potassium channels in vascular smooth muscle cells.Physiological reviews · 2026Review
- The Potential of a Protein Model Synthesized Absent of Methionine.Molecules (Basel, Switzerland) · 2022Review
- The Large-Conductance, Calcium-Activated Potassium Channel: A Big Key Regulator of Cell Physiology.Frontiers in physiology · 2021Review
- Biological sulfur in the blood cells of Ascidia ceratodes: XAS spectroscopy and a cellular-enzymatic hypothesis for vanadium reduction in the ascidians.Journal of inorganic biochemistry · 2020Article
- Oxidative Stress and Maxi Calcium-Activated Potassium (BK) Channels.Biomolecules · 2015Review
- Redox regulation of ion channels in the pulmonary circulation.Antioxidants & redox signaling · 2015Review
- Regulation of ion channels by pyridine nucleotides.Circulation research · 2013Review
- Hypoxic pulmonary vasoconstriction.Physiological reviews · 2012Review
- Hypoxic pulmonary vasoconstriction: mechanisms of oxygen-sensing.Current opinion in anaesthesiology · 2011Review
- Hydrogen sulfide increases calcium-activated potassium (BK) channel activity of rat pituitary tumor cells.Pflugers Archiv : European journal of physiology · 2010Article
- Mitochondria, oxidative stress, and temporal lobe epilepsy.Epilepsy research · 2010Review
- Sodium (2-sulfonatoethyl) methanethiosulfonate prevents S-nitroso-L-cysteine activation of Ca2+-activated K+ (BKCa) channels in myocytes of the guinea-pig taenia caeca.British journal of pharmacology · 2003Article
- Reduced to oxidized glutathione ratios and oxygen sensing in calf and rabbit carotid body chemoreceptor cells.The Journal of physiology · 2001Article
- Oxidative regulation of large conductance calcium-activated potassium channels.The Journal of general physiology · 2001Article
- Regulation of cell function by methionine oxidation and reduction.The Journal of physiology · 2001Review
- Voltage and Ca2+ activation of single large-conductance Ca2+-activated K+ channels described by a two-tiered allosteric gating mechanism.The Journal of general physiology · 2000Article
- Nitric oxide and thiol reagent modulation of Ca2+-activated K+ (BKCa) channels in myocytes of the guinea-pig taenia caeci.The Journal of physiology · 2000Article
- Ca2+-dependent gating mechanisms for dSlo, a large-conductance Ca2+-activated K+ (BK) channel.Biophysical journal · 1999Article
- Contribution of Ca2+-activated K+ channels and non-selective cation channels to membrane potential of pulmonary arterial smooth muscle cells of the rabbit.The Journal of physiology · 1999Article
- Kinetic structure of large-conductance Ca2+-activated K+ channels suggests that the gating includes transitions through intermediate or secondary states. A mechanism for flickers.The Journal of general physiology · 1998Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. The effects of intracellular redox couples were investigated on the activation by voltage, Ca2+ and NS 1619 of maxi-K channels in enzymatically isolated smooth muscle cells from large pulmonary arteries of rabbits. 2. In inside-out membrane patches, maxi-K channels were characterized by a single-channel conductance of 266 pS in symmetrical 140 mM KCl solutions. The relationship between the open-state probability (Po) and the membrane potential could be fitted to the Boltzmann equation. The activating action of intracellular Ca2+ was reversible, concentration dependent, and was manifested as the reduction in the voltage necessary to half-activate the channel (V1/2) with no change in the slope factor. NS 1619 also predisposed the maxi-K channel to open at more hyperpolarized membrane potentials. 3. The oxidizing agent 5,5'-dithio-bis(2-nitrobenzoic acid) (DTNB, 1 mM) activated maxi-K channels by inducing a negative shift of the activity-voltage curve, while the reducing agent 2-hydroxy-1-ethanethiol (beta-mercaptoethanol) (BME, 1 mM) had no effect. DTNB increased the efficacy of Ca2+ in activating maxi-K channels. The action of DTNB was not reversible upon wash-out, but could be counteracted by BME. 4. Maxi-K channel activity was unaffected by other oxidizing agents, such as NAD (2 mM) and glutathione disulphide (GSSG, 5 mM), or by their reduced forms (NADH and GSH). Mg-ATP (0.1 and 1 mM) increased the channel activity in a dose-dependent manner, while guanine nucleotides (100 microM GTP gamma S, 500 microM GDP and 200 microM GDP beta S) had no effect. 5. Our data suggest that a change in the intracellular redox state, which would be expected during acute hypoxia, does not alter the activity of maxi-K channels of large pulmonary artery smooth muscle cells. The sulfhydryl-specific redox reagents (DTNB and BME) must act through another regulatory mechanism.
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