ReviewJournal of applied physiology (Bethesda, Md. : 1985)2015
Neurogenic mechanisms underlying the rapid onset of sympathetic responses to intermittent hypoxia.
Review in Journal of applied physiology (Bethesda, Md. : 1985), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
What it found
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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.
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Who cites it
23 citing papers in PubMed, 35 citations in OpenAlex.
- The development but not the maintenance of phrenic and sympathetic long-term facilitation after acute intermittent hypoxia requires nucleus tractus solitarii HExperimental neurology · 2025Article
- Cluster Headache and Hypoxia: Breathing New Life into an Old Theory, with Novel Implications.Neurology international · 2024Review
- Dual Approach to Depression: The Combined Efficacy of Intermittent Hypoxia and Fluoxetine in Modulating Behavioral and Inflammatory Responses.Biomedicines · 2024Article
- Pulmonary Vascular Responses to Chronic Intermittent Hypoxia in a Guinea Pig Model of Obstructive Sleep Apnea.International journal of molecular sciences · 2024Article
- The Effects of Volatile Anesthetics on Renal Sympathetic and Phrenic Nerve Activity during Acute Intermittent Hypoxia in Rats.Biomedicines · 2024Article
- Nucleus tractus solitarii is required for the development and maintenance of phrenic and sympathetic long-term facilitation after acute intermittent hypoxia.Frontiers in physiology · 2023Article
- Chronic intermittent hypoxia enhances glycinergic inhibition in nucleus tractus solitarius.Journal of neurophysiology · 2022Article
- Carotid body chemoreceptors: physiology, pathology, and implications for health and disease.Physiological reviews · 2021Review
- The protective role of SOD1 overexpression in central mediation of bradycardia following chronic intermittent hypoxia in mice.American journal of physiology. Regulatory, integrative and comparative physiology · 2021Article
- Pentobarbital Anesthesia Suppresses the Glucose Response to Acute Intermittent Hypoxia in Rat.Frontiers in physiology · 2021Article
- Recent Advances in Studies on the Role of Neuroendocrine Disorders in Obstructive Sleep Apnea-Hypopnea Syndrome-Related Atherosclerosis.Nature and science of sleep · 2021Review
- Sympathetic neural recruitment strategies following acute intermittent hypoxia in humans.American journal of physiology. Regulatory, integrative and comparative physiology · 2020Article
- Central AT1 receptor signaling by circulating angiotensin II is permissive to acute intermittent hypoxia-induced sympathetic neuroplasticity.Journal of applied physiology (Bethesda, Md. : 1985) · 2020Article
- Astrocytes Modulate Baroreflex Sensitivity at the Level of the Nucleus of the Solitary Tract.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Caspase lesions of PVN-projecting MnPO neurons block the sustained component of CIH-induced hypertension in adult male rats.American journal of physiology. Heart and circulatory physiology · 2020Article
- Glucose-Lowering by Leptin in the Absence of Insulin Does Not Fully Rely on the Central Melanocortin System in Male Mice.Endocrinology · 2019Article
- Chronic intermittent hypoxia disrupts cardiorespiratory homeostasis and gut microbiota composition in adult male guinea-pigs.EBioMedicine · 2018Article
- Regulation of sympathetic vasomotor activity by the hypothalamic paraventricular nucleus in normotensive and hypertensive states.American journal of physiology. Heart and circulatory physiology · 2018Review
- CRHR2 (Corticotropin-Releasing Hormone Receptor 2) in the Nucleus of the Solitary Tract Contributes to Intermittent Hypoxia-Induced Hypertension.Hypertension (Dallas, Tex. : 1979) · 2018Article
- Hypothalamic PVN contributes to acute intermittent hypoxia-induced sympathetic but not phrenic long-term facilitation.Journal of applied physiology (Bethesda, Md. : 1985) · 2018Article
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
Abstract
Sleep apnea (SA) leads to metabolic abnormalities and cardiovascular dysfunction. Rodent models of nocturnal intermittent hypoxia (IH) are used to mimic arterial hypoxemias that occur during SA. This mini-review focuses on our work examining central nervous system (CNS) mechanisms whereby nocturnal IH results in increased sympathetic nerve discharge (SND) and hypertension (HTN) that persist throughout the 24-h diurnal period. Within the first 1-2 days of IH, arterial pressure (AP) increases even during non-IH periods of the day. Exposure to IH for 7 days biases nucleus tractus solitarius (NTS) neurons receiving arterial chemoreceptor inputs toward increased discharge, providing a substrate for persistent activation of sympathetic outflow. IH HTN is blunted by manipulations that reduce angiotensin II (ANG II) signaling within the forebrain lamina terminalis suggesting that central ANG II supports persistent IH HTN. Inhibition of the hypothalamic paraventricular nucleus (PVN) reduces ongoing SND and acutely lowers AP in IH-conditioned animals. These findings support a role for the PVN, which integrates information ascending from NTS and descending from the lamina terminalis, in sustaining IH HTN. In summary, our findings indicate that IH rapidly and persistently activates a central circuit that includes the NTS, forebrain lamina terminalis, and the PVN. Our working model holds that NTS neuromodulation increases transmission of arterial chemoreceptor inputs, increasing SND via connections with PVN and rostral ventrolateral medulla. Increased circulating ANG II sensed by the lamina terminalis generates yet another excitatory drive to PVN. Together with adaptations intrinsic to the PVN, these responses to IH support rapid onset neurogenic HTN.
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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.