ReviewRespiratory physiology & neurobiology2015
Neuromolecular mechanisms mediating the effects of chronic intermittent hypoxia on adrenal medulla.
Review in Respiratory physiology & neurobiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed, 14 citations in OpenAlex.
- Adaptive remodeling of rat adrenomedullary stimulus-secretion coupling in a chronic hypertensive environment.Cellular and molecular life sciences : CMLS · 2024Article
- Feasibility of Using Daily Home High-Flow Nasal Therapy in COPD Patients Following a Recent COPD Hospitalization.Chronic obstructive pulmonary diseases (Miami, Fla.) · 2022Article
- Hypoxia-regulated catecholamine secretion in chromaffin cells.Cell and tissue research · 2018Review
- Guinea Pig as a Model to Study the Carotid Body Mediated Chronic Intermittent Hypoxia Effects.Frontiers in physiology · 2018Article
- Chronic intermittent hypoxia and obstructive sleep apnea: an experimental and clinical approach.Hypoxia (Auckland, N.Z.) · 2016Review
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 1 institution in 1 country.
Funding
Abstract
Sleep disordered breathing (SDB) with recurrent apnea is a major health problem affecting several million adult men and women. Humans with SDB are prone to develop hypertension. Studies on rodents established that exposure to chronic intermittent hypoxia (CIH) alone is sufficient to induce hypertension similar to that seen in patients with SDB. Available evidence from studies on experimental animals suggests that catecholamines secreted from adrenal medulla (AM), an end-organ of the sympathetic nervous system is a major contributor to CIH-induced hypertension. In this article, we present an overview of our current understanding on how CIH reconfigures AM function and highlight recent findings on the underlying cellular and molecular mechanisms.
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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.