ArticleThe Journal of physiology1996
Oxidant stress activates a non-selective cation channel responsible for membrane depolarization in calf vascular endothelial cells.
Article in The Journal of physiology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed, 61 citations in OpenAlex.
- Quantification of mitochondrial membrane potential in the isolated rat lung using rhodamine 6G.Journal of applied physiology (Bethesda, Md. : 1985) · 2020Article
- Reactive oxygen species increase neuronal excitability via activation of nonspecific cation channel in rat medullary dorsal horn neurons.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2017Article
- On the role of endothelial TRPC3 channels in endothelial dysfunction and cardiovascular disease.Cardiovascular & hematological agents in medicinal chemistry · 2012Review
- Redox regulation of endothelial canonical transient receptor potential channels.Antioxidants & redox signaling · 2011Review
- Quantifying mitochondrial and plasma membrane potentials in intact pulmonary arterial endothelial cells based on extracellular disposition of rhodamine dyes.American journal of physiology. Lung cellular and molecular physiology · 2011Article
- Hydrogen peroxide removes TRPM4 current desensitization conferring increased vulnerability to necrotic cell death.The Journal of biological chemistry · 2010Article
- The role of nitric oxide and reactive oxygen species in the positive inotropic response to mechanical stretch in the mammalian myocardium.Biochimica et biophysica acta · 2009Article
- Functional consequences of oxidative membrane damage.The Journal of membrane biology · 2005Review
- Heme oxygenase-2 products activate IKCa: role of CO and iron in guinea pig portal vein smooth muscle cells.Journal of muscle research and cell motility · 2004Article
- Intercellular signalling within vascular cells under high D-glucose involves free radical-triggered tyrosine kinase activation.Diabetologia · 2003Article
- Negative feedback regulation of reactive oxygen species on AT1 receptor gene expression.British journal of pharmacology · 2000Article
- Activation of a Ca2+-permeable cation channel by two different inducers of apoptosis in a human prostatic cancer cell line.The Journal of physiology · 1999Article
- Reduced glutathione inhibits beta-NAD+-activated non-selective cation currents in the CRI-G1 rat insulin-secreting cell line.The Journal of physiology · 1999Article
- Near-visible ultraviolet light induces a novel ubiquitous calcium-permeable cation current in mammalian cell lines.The Journal of physiology · 1998Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
1. In vascular endothelial cells, oxidant stress increases cell Na+ content and inhibits the agonist-stimulated influx of external Ca2+. Further, oxidant stress increases uptake of Ca2+ into otherwise quiescent endothelial cells. To determine the mechanism responsible for altered Na+ and Ca2+ homeostasis, the present study examined the effect of oxidant stress on ionic current and channel activity in calf pulmonary artery endothelial cells. 2. Voltage-clamped control cells had a zero-current potential of -60 mV. Incubation of cells with the oxidant tert-butylhydroperoxide (tBuOOH; 0.4 mM, 1 h) caused depolarization to -4 mV and activation of ionic current equally selective for Na+ and K+. 3. Cell-attached membrane patches made on tBuOOH-treated cells contained ion channels that had a bidirectional conductance of 30 pS and that were not present in patches from control cells. Inside-out patches excised from oxidant-treated cells showed the channel to be equally selective for Na+ and K+ and to allow inward Ca2+ current. 4. Oxidant-activated channels were observed to display two gating modalities that were further evident during analysis of single-channel open probability. Neither modality was significantly affected by altering internal [Ca2+] (1 microM-10 nM). 5. Activation of non-selective channels provides a possible mechanism by which oxidants may increase endothelial cell Na+ content. Channel permeability to Ca2+ may account in part for the elevation of cytosolic free [Ca2+] that occurs in oxidant-treated cells. 6. Channel activation is associated with membrane depolarization, a mechanism that may contribute to oxidant inhibition of the agonist-stimulated Ca2+ influx pathway.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.