ArticleThe Journal of physiology2005
Mobilization of sarcoplasmic reticulum stores by hypoxia leads to consequent activation of capacitative Ca2+ entry in isolated canine pulmonary arterial smooth muscle cells.
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 37 papers.
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Who cites it
37 citing papers in PubMed, 72 citations in OpenAlex.
- Altitude hypoxia and hypoxemia: pathogenesis and management.Signal transduction and targeted therapy · 2026Review
- Role of ryanodine receptor 2 and FK506-binding protein 12.6 dissociation in pulmonary hypertension.The Journal of general physiology · 2023Article
- Important Role of Sarcoplasmic Reticulum CaAntioxidants & redox signaling · 2020Article
- Endoplasmic reticulum Ca2+ release causes Rieske iron-sulfur protein-mediated mitochondrial ROS generation in pulmonary artery smooth muscle cells.Bioscience reports · 2019Article
- Lung Circulation.Comprehensive Physiology · 2016Review
- Role of ASIC1 in the development of chronic hypoxia-induced pulmonary hypertension.American journal of physiology. Heart and circulatory physiology · 2014Article
- Prenatal programming of pulmonary hypertension induced by chronic hypoxia or ductal ligation in sheep.Pulmonary circulation · 2013Review
- Acute hypoxia activates store-operated Ca(2+) entry and increases intracellular Ca(2+) concentration in rat distal pulmonary venous smooth muscle cells.Journal of thoracic disease · 2013Article
- Hypoxic pulmonary vasoconstriction in the absence of pretone: essential role for intracellular Ca2+ release.The Journal of physiology · 2013Article
- Antenatal hypoxia and pulmonary vascular function and remodeling.Current vascular pharmacology · 2013Review
- Effect of chronic perinatal hypoxia on the role of rho-kinase in pulmonary artery contraction in newborn lambs.American journal of physiology. Regulatory, integrative and comparative physiology · 2013Article
- Effect of Yifei Huoxue Granule on the proliferation of rat pulmonary artery smooth muscle cells upon exposure to chronic hypoxic conditions in vitro.Chinese journal of integrative medicine · 2012Article
- Ca2+ responses of pulmonary arterial myocytes to acute hypoxia require release from ryanodine and inositol trisphosphate receptors in sarcoplasmic reticulum.American journal of physiology. Lung cellular and molecular physiology · 2012Article
- Hypoxic pulmonary vasoconstriction.Physiological reviews · 2012Review
- Long-term maternal hypoxia: the role of extracellular Ca2+ entry during serotonin-mediated contractility in fetal ovine pulmonary arteries.Reproductive sciences (Thousand Oaks, Calif.) · 2011Article
- Hypoxia. 4. Hypoxia and ion channel function.American journal of physiology. Cell physiology · 2011Review
- Hypoxia induces intracellular Ca2+ release by causing reactive oxygen species-mediated dissociation of FK506-binding protein 12.6 from ryanodine receptor 2 in pulmonary artery myocytes.Antioxidants & redox signaling · 2011Article
- Role of ROS signaling in differential hypoxic Ca2+ and contractile responses in pulmonary and systemic vascular smooth muscle cells.Respiratory physiology & neurobiology · 2010Article
- Interactions between calcium and reactive oxygen species in pulmonary arterial smooth muscle responses to hypoxia.Respiratory physiology & neurobiology · 2010Review
- ROS-dependent signaling mechanisms for hypoxic Ca(2+) responses in pulmonary artery myocytes.Antioxidants & redox signaling · 2010Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Capacitative Ca2+ entry (CCE) has been speculated to contribute to Ca2+ influx during hypoxic pulmonary vasoconstriction (HPV). The aim of the present study was to directly test if acute hypoxia causes intracellular Ca2+ concentration ([Ca2+]i) rises through CCE in canine pulmonary artery smooth muscle cells (PASMCs). In PASMCs loaded with fura-2, hypoxia produced a transient rise in [Ca2+]i in Ca2+-free solution, indicating Ca2+ release from the intracellular Ca2+ stores. Subsequent addition of 2 mm Ca2+ in hypoxia elicited a sustained rise in [Ca2+]i, which was partially inhibited by 10 microm nisoldipine. The dihydropyridine-insensitive rise in [Ca2+]i was due to increased Ca2+ influx, because it was abolished in Ca2+-free solution and hypoxia was shown to significantly enhance the rate of Mn2+ quench of fura-2 fluorescence. The dihyropyridine-insensitive rise in [Ca2+]i and the increased rate of Mn2+ quench of fura-2 fluorescence were inhibited by 50 microm SKF 96365 and 500 microm Ni2+, but not by 100 microm La3+ or 100 microm Gd3+, exhibiting pharmacological properties characteristic of CCE. In addition, predepletion of the intracellular Ca2+ stores inhibited the rise in [Ca2+]i induced by hypoxia. These results provide the first direct evidence that acute hypoxia, by causing Ca2+ release from the intracellular stores, activates CCE in isolated canine PASMCs, which may contribute to HPV.
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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.