ArticleThe Journal of physiology2005
Down regulation of Kv3.4 channels by chronic hypoxia increases acute oxygen sensitivity in rabbit carotid body.
Article in The Journal of physiology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed, 47 citations in OpenAlex.
- Article
- The new KNeural regeneration research · 2020Article
- Synthesis and Pharmacological Evaluation of a Novel Peptide Based onFrontiers in chemistry · 2019Article
- Kv3.1 and Kv3.4, Are Involved in Cancer Cell Migration and Invasion.International journal of molecular sciences · 2018Article
- Carotid Body Type-I Cells Under Chronic Sustained Hypoxia: Focus on Metabolism and Membrane Excitability.Frontiers in physiology · 2018Article
- Kv3.4 is modulated by HIF-1α to protect SH-SY5Y cells against oxidative stress-induced neural cell death.Scientific reports · 2017Article
- Single cell transcriptome analysis of mouse carotid body glomus cells.The Journal of physiology · 2016Article
- Enhanced Firing in NTS Induced by Short-Term Sustained Hypoxia Is Modulated by Glia-Neuron Interaction.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Short-term sustained hypoxia induces changes in the coupling of sympathetic and respiratory activities in rats.The Journal of physiology · 2014Article
- Evidence of accelerated evolution and ectodermal-specific expression of presumptive BDS toxin cDNAs from Anemonia viridis.Marine drugs · 2013Article
- A possible role for systemic hypoxia in the reactive component of pulmonary hypertension in heart failure.Journal of cardiac failure · 2013Article
- Chronic hypoxia-induced acid-sensitive ion channel expression in chemoafferent neurons contributes to chemoreceptor hypersensitivity.American journal of physiology. Lung cellular and molecular physiology · 2011Article
- From oncoproteins/tumor suppressors to microRNAs, the newest therapeutic targets for pulmonary arterial hypertension.Journal of molecular medicine (Berlin, Germany) · 2011Review
- Pathophysiology of sleep apnea.Physiological reviews · 2010Review
- Breathing at high altitude.Cellular and molecular life sciences : CMLS · 2009Review
- A role for DPPX modulating external TEA sensitivity of Kv4 channels.The Journal of general physiology · 2008Article
- Carotid body function in heart failure.Respiratory physiology & neurobiology · 2007Review
- Enhanced sensitivity of Kv channels to hypoxia in the rabbit carotid body in heart failure: role of angiotensin II.The Journal of physiology · 2006Article
- Modulation of Kv3 subfamily potassium currents by the sea anemone toxin BDS: significance for CNS and biophysical studies.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2005Article
- Comparative gene expression profile of mouse carotid body and adrenal medulla under physiological hypoxia.The Journal of physiology · 2005Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The carotid body (CB) chemoreceptors participate in the ventilatory responses to acute and chronic hypoxia (CH). Arterial hypoxaemia increases breathing within seconds, and CB chemoreceptors are the principal contributors to this reflex hyperventilatory response. Acute hypoxia induces depolarization of CB chemoreceptors by inhibiting certain K+ channels, but the role of these channels in CH, as in high-altitude acclimatization, is less known. Here we explored the effects of prolonged (24-48 h) hypoxic exposure of rabbit CB chemoreceptor cells in primary cultures on the voltage-dependent K+ currents and on their response to acute hypoxia. We found that CH induces a decrease in the amplitude of outward K+ currents due to a reduction in a fast-inactivating BDS- and highly TEA-sensitive component of the current. In spite of this effect, acute hypoxic inhibition of K+ currents is increased in CH cultures, as well as hypoxia-induced depolarization. These data suggest that downregulation of this component (that does not contribute to the oxygen-sensitive K+ current (IKO2) participates in the hypoxic sensitization. Pharmacological, immunocytochemical and quantitative PCR (qPCR) experiments demonstrate that CH-induced decrease in outward K+ currents is due to a downregulation of the expression of Kv3.4 channels. Taken together, our results suggest that CH sensitization in rabbit CB could be achieved by an increase in the relative contribution of IKO2 to the outward K+ current as a consequence of the decreased expression of the oxygen-insensitive component of the current. We conclude that acute and chronic hypoxia can exert their effects acting on different molecular targets.
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.