ArticleAmerican journal of physiology. Cell physiology2012
Endogenous H2S is required for hypoxic sensing by carotid body glomus cells.
Article in American journal of physiology. Cell physiology, 2012. 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, 69 citations in OpenAlex.
- The Role of Hydrogen Sulfide in the Regulation of the Pulmonary Vasculature in Health and Disease.Antioxidants (Basel, Switzerland) · 2025Review
- Signal Transduction Pathway Mediating Carotid Body Dependent Sympathetic Activation and Hypertension by Chronic Intermittent Hypoxia.Function (Oxford, England) · 2025Article
- Hypoxia sensing requires HScience advances · 2023Article
- Pathophysiological mechanisms and therapeutic approaches in obstructive sleep apnea syndrome.Signal transduction and targeted therapy · 2023Review
- Neurochemical Anatomy of the Mammalian Carotid Body.Advances in anatomy, embryology, and cell biology · 2023Article
- A Case for Hydrogen Sulfide Metabolism as an Oxygen Sensing Mechanism.Antioxidants (Basel, Switzerland) · 2021Review
- HJournal of clinical medicine · 2021Article
- Gaseous transmitter regulation of hypoxia-evoked catecholamine secretion from murine adrenal chromaffin cells.Journal of neurophysiology · 2021Article
- Simulated sleep apnea alters hydrogen sulfide regulation of blood flow and pressure.American journal of physiology. Heart and circulatory physiology · 2021Article
- Olfactory receptor 78 participates in carotid body response to a wide range of low OJournal of neurophysiology · 2020Article
- Hydroxycobalamin Reveals the Involvement of Hydrogen Sulfide in the Hypoxic Responses of Rat Carotid Body Chemoreceptor Cells.Antioxidants (Basel, Switzerland) · 2019Article
- HRespiratory physiology & neurobiology · 2019Article
- Reactive oxygen radicals and gaseous transmitters in carotid body activation by intermittent hypoxia.Cell and tissue research · 2018Review
- Recent advances in understanding the physiology of hypoxic sensing by the carotid body.F1000Research · 2018Review
- Calpain activation by ROS mediates human ether-a-go-go-related gene protein degradation by intermittent hypoxia.American journal of physiology. Cell physiology · 2016Article
- An emerging role for gasotransmitters in the control of breathing and ionic regulation in fish.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2016Review
- CaV3.2 T-type Ca2+ channels mediate the augmented calcium influx in carotid body glomus cells by chronic intermittent hypoxia.Journal of neurophysiology · 2016Article
- Oxygen Sensing and Homeostasis.Physiology (Bethesda, Md.) · 2015Review
- Hydrogen sulfide and hypoxia-induced changes in TASK (K2P3/9) activity and intracellular Ca(2+) concentration in rat carotid body glomus cells.Respiratory physiology & neurobiology · 2015Article
- Protein kinase G-regulated production of H2S governs oxygen sensing.Science signaling · 2015Article
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8 authors at 4 institutions in 1 country.
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Abstract
H(2)S generated by the enzyme cystathionine-γ-lyase (CSE) has been implicated in O(2) sensing by the carotid body. The objectives of the present study were to determine whether glomus cells, the primary site of hypoxic sensing in the carotid body, generate H(2)S in an O(2)-sensitive manner and whether endogenous H(2)S is required for O(2) sensing by glomus cells. Experiments were performed on glomus cells harvested from anesthetized adult rats as well as age and sex-matched CSE(+/+) and CSE(-/-) mice. Physiological levels of hypoxia (Po(2) ∼30 mmHg) increased H(2)S levels in glomus cells, and dl-propargylglycine (PAG), a CSE inhibitor, prevented this response in a dose-dependent manner. Catecholamine (CA) secretion from glomus cells was monitored by carbon-fiber amperometry. Hypoxia increased CA secretion from rat and mouse glomus cells, and this response was markedly attenuated by PAG and in cells from CSE(-/-) mice. CA secretion evoked by 40 mM KCl, however, was unaffected by PAG or CSE deletion. Exogenous application of a H(2)S donor (50 μM NaHS) increased cytosolic Ca(2+) concentration ([Ca(2+)](i)) in glomus cells, with a time course and magnitude that are similar to that produced by hypoxia. [Ca(2+)](i) responses to NaHS and hypoxia were markedly attenuated in the presence of Ca(2+)-free medium or cadmium chloride, a pan voltage-gated Ca(2+) channel blocker, or nifedipine, an L-type Ca(2+) channel inhibitor, suggesting that both hypoxia and H(2)S share common Ca(2+)-activating mechanisms. These results demonstrate that H(2)S generated by CSE is a physiologic mediator of the glomus cell's response to hypoxia.
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