ArticleExperimental physiology2013
Role of oxidative stress-induced endothelin-converting enzyme activity in the alteration of carotid body function by chronic intermittent hypoxia.
Article in Experimental physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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23 citing papers in PubMed, 47 citations in OpenAlex.
- Effect of endothelin-1 on the blood pressure response to acute hypoxia and hyperoxia in healthy young men.Physiological reports · 2024Trial
- Oxygen, carbon dioxide, and nitric oxide: role in the pathophysiology of obstructive sleep apnea.Medical gas research · 2027Review
- Sleep, Neural Circulatory Control, and Cardiovascular Disease: A Mechanistic Review.Arteriosclerosis, thrombosis, and vascular biology · 2026Review
- Advancements in the neurocirculatory reflex response to hypoxia.American journal of physiology. Regulatory, integrative and comparative physiology · 2024Review
- On the origins of sleep disordered breathing, cardiorespiratory and metabolic dysfunction: which came first, the chicken or the egg?The Journal of physiology · 2023Article
- Pathophysiological mechanisms and therapeutic approaches in obstructive sleep apnea syndrome.Signal transduction and targeted therapy · 2023Review
- Adaptive cardiorespiratory changes to chronic continuous and intermittent hypoxia.Handbook of clinical neurology · 2022Review
- Carotid body chemoreceptors: physiology, pathology, and implications for health and disease.Physiological reviews · 2021Review
- Comparative morphological and molecular studies on the oxygen-chemoreceptive cells in the carotid body and fish gills.Cell and tissue research · 2021Review
- Simulated sleep apnea alters hydrogen sulfide regulation of blood flow and pressure.American journal of physiology. Heart and circulatory physiology · 2021Article
- Hypoxia-inducible factors and obstructive sleep apnea.The Journal of clinical investigation · 2020Review
- Growth Factors in the Carotid Body-An Update.International journal of molecular sciences · 2020Review
- G-Protein-Coupled Receptor (GPCR) Signaling in the Carotid Body: Roles in Hypoxia and Cardiovascular and Respiratory Disease.International journal of molecular sciences · 2020Review
- Receptor-Receptor Interactions of G Protein-Coupled Receptors in the Carotid Body: A Working Hypothesis.Frontiers in physiology · 2018Article
- Role of Carotid Body in Intermittent Hypoxia-Related Hypertension.Current hypertension reports · 2017Review
- Oxidative stress augments chemoreflex sensitivity in rats exposed to chronic intermittent hypoxia.Respiratory physiology & neurobiology · 2016Article
- H2S production by reactive oxygen species in the carotid body triggers hypertension in a rodent model of sleep apnea.Science signaling · 2016Article
- Carotid body chemoreflex: a driver of autonomic abnormalities in sleep apnoea.Experimental physiology · 2016Review
- N-Acetylcysteine reduces hyperacute intermittent hypoxia-induced sympathoexcitation in human subjects.Experimental physiology · 2016Article
- Carotid body oxygen sensing and adaptation to hypoxia.Pflugers Archiv : European journal of physiology · 2016Review
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6 authors at 2 institutions in 1 country.
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Abstract
Chronic intermittent hypoxia (CIH) leads to remodelling of the carotid body function, manifested by an augmented sensory response to hypoxia and induction of sensory long-term facilitation (LTF). It was proposed that endothelin-1 (ET-1) contributes to CIH-induced hypoxic hypersensitivity of the carotid body. The objectives of the present study were as follows: (i) to delineate the mechanisms by which CIH upregulates ET-1 expression in the carotid body; and (ii) to assess whether ET-1 also contributes to sensory LTF. Experiments were performed on adult, male rats exposed to alternating cycles of 5% O2 (15 s) and room air (5 min), nine episodes per hour and 8 h per day for 10 days. Chronic intermittent hypoxia increased ET-1 levels in glomus cells without significantly altering prepro-endothelin-1 mRNA levels. The activity of endothelin-converting enzyme increased with concomitant elevation of ET-1 levels in CIH-exposed carotid bodies, and MnTMPyP, a membrane-permeable antioxidant, prevented these effects. Hypoxia facilitated ET-1 release from CIH-treated carotid bodies, which is a prerequisite for activation of ET receptors; however, hypoxia had no effect on ET-1 release from control carotid bodies. In CIH-exposed carotid bodies, mRNAs encoding ETA receptor were upregulated, and an ETA receptor-specific antagonist abolished CIH-induced hypersensitivity of the hypoxic response, whereas it had no effect on the sensory LTF. These results suggest that ECE-dependent increased production of ET-1 coupled with hypoxia-evoked ET-1 release and the ensuing ETA receptor activation mediate the CIH-induced carotid body hypersensitivity to hypoxia, but the ETA signalling pathway is not associated with sensory LTF elicited by CIH.
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