ArticleJournal of neurophysiology2009
Neonatal intermittent hypoxia leads to long-lasting facilitation of acute hypoxia-evoked catecholamine secretion from rat chromaffin cells.
Article in Journal of neurophysiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 53 citations in OpenAlex.
- Review
- A Consequence of Immature Breathing induces Persistent Changes in Hippocampal Synaptic Plasticity and Behavior: A Role of Pro-Oxidant State and NMDA Receptor Imbalance.bioRxiv : the preprint server for biology · 2023Article
- A consequence of immature breathing induces persistent changes in hippocampal synaptic plasticity and behavior: a role of prooxidant state and NMDA receptor imbalance.Frontiers in molecular neuroscience · 2023Article
- Protein phosphatase 1 regulates reactive oxygen species-dependent degradation of histone deacetylase 5 by intermittent hypoxia.American journal of physiology. Cell physiology · 2022Article
- Gaseous transmitter regulation of hypoxia-evoked catecholamine secretion from murine adrenal chromaffin cells.Journal of neurophysiology · 2021Article
- Respiratory rhythm generation, hypoxia, and oxidative stress-Implications for development.Respiratory physiology & neurobiology · 2019Review
- Long-term facilitation of catecholamine secretion from adrenal chromaffin cells of neonatal rats by chronic intermittent hypoxia.Journal of neurophysiology · 2019Article
- Chromaffin Cells of the Adrenal Medulla: Physiology, Pharmacology, and Disease.Comprehensive Physiology · 2019Article
- Neural Activation of Molecular Circuitry in Intermittent Hypoxia.Current opinion in physiology · 2019Article
- DNA methylation in the central and efferent limbs of the chemoreflex requires carotid body neural activity.The Journal of physiology · 2018Article
- Epigenetic regulation of redox state mediates persistent cardiorespiratory abnormalities after long-term intermittent hypoxia.The Journal of physiology · 2017Article
- Carotid body chemoreflex: a driver of autonomic abnormalities in sleep apnoea.Experimental physiology · 2016Review
- Cardiorespiratory events in preterm infants: interventions and consequences.Journal of perinatology : official journal of the California Perinatal Association · 2016Review
- Calpain activation by ROS mediates human ether-a-go-go-related gene protein degradation by intermittent hypoxia.American journal of physiology. Cell physiology · 2016Article
- Peripheral chemoreception and arterial pressure responses to intermittent hypoxia.Comprehensive Physiology · 2015Review
- Neuromolecular mechanisms mediating the effects of chronic intermittent hypoxia on adrenal medulla.Respiratory physiology & neurobiology · 2015Review
- HIF-1α activation by intermittent hypoxia requires NADPH oxidase stimulation by xanthine oxidase.PloS one · 2015Article
- Epigenetic Regulation of Carotid Body Oxygen Sensing: Clinical Implications.Advances in experimental medicine and biology · 2015Review
- Neuropeptide y gates a stress-induced, long-lasting plasticity in the sympathetic nervous system.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Developmental programming of O(2) sensing by neonatal intermittent hypoxia via epigenetic mechanisms.Respiratory physiology & neurobiology · 2013Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The objective of the present study was to examine the effects of intermittent hypoxia (IH) and sustained hypoxia (SH) on hypoxia-evoked catecholamine (CA) secretion from chromaffin cells in neonatal rats and assess the underlying mechanism(s). Experiments were performed on rat pups exposed to either IH (15-s hypoxia/5-min normoxia; 8 h/day) or SH (hypobaric hypoxia, 0.4 atm) or normoxia (controls) from P0 to P5. IH treatment facilitated hypoxia-evoked CA secretion and elevations in the intracellular calcium ion concentration ([Ca(2+)](i)) and these responses were attenuated, but not abolished, by treatments designed to eliminate Ca(2+) flux into cells (Ca(2+)-free medium or Cd(2+)), indicating that intracellular Ca(2+) stores were augmented by IH. Norepinephrine (NE) and epinephrine (E) levels of adrenal medullae were elevated in IH-treated pups. IH treatment increased reactive oxygen species (ROS) production in adrenal medullae and antioxidant treatment prevented IH-induced facilitation of CA secretion, elevations in [Ca(2+)](i) by hypoxia, and the up-regulation of NE and E. The effects of neonatal IH treatment on hypoxia-induced CA secretion and elevation in [Ca(2+)](i), CA, and ROS levels persisted in rats reared under normoxia for >30 days. In striking contrast, chromaffin cells from SH-treated animals exhibited attenuated hypoxia-evoked CA secretion. In SH-treated cells hypoxia-evoked elevations in [Ca(2+)](i), NE and E contents, and ROS levels were comparable with controls. These observations demonstrate that: 1) neonatal IH and SH evoke opposite effects on hypoxia-evoked CA secretion from chromaffin cells, 2) ROS signaling mediates the faciltatory effects of IH, and 3) the effects of neonatal IH on chromaffin cells persist into adult life.
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