ArticleAmerican journal of physiology. Cell physiology2015
CaV3.2 T-type Ca²⁺ channels in H₂S-mediated hypoxic response of the carotid body.
Article in American journal of physiology. Cell physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 19 citations in OpenAlex.
- The cystathionine-γ-lyase inhibitor DL-propargylglycine augments the ability of L-cysteine ethyl ester to overcome the adverse effects of morphine on breathing.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- Gas-powered extracellular vesicles promote bone regeneration.Extracellular vesicles and circulating nucleic acids · 2025Article
- Pathophysiological mechanisms and therapeutic approaches in obstructive sleep apnea syndrome.Signal transduction and targeted therapy · 2023Review
- Hypoxia releases S-nitrosocysteine from carotid body glomus cells-relevance to expression of the hypoxic ventilatory response.Frontiers in pharmacology · 2023Article
- CaAmerican journal of physiology. Cell physiology · 2020Article
- Hydroxycobalamin Reveals the Involvement of Hydrogen Sulfide in the Hypoxic Responses of Rat Carotid Body Chemoreceptor Cells.Antioxidants (Basel, Switzerland) · 2019Article
- Influence of propofol on isolated neonatal rat carotid body glomus cell response to hypoxia and hypercapnia.Respiratory physiology & neurobiology · 2019Article
- Sulfur-containing gaseous signal molecules, ion channels and cardiovascular diseases.British journal of pharmacology · 2018Review
- Single cell transcriptome analysis of mouse carotid body glomus cells.The Journal of physiology · 2016Article
- Hyperpolarization-activated cation and T-type calcium ion channel expression in porcine and human renal pacemaker tissues.Journal of anatomy · 2016Article
- Calpain activation by ROS mediates human ether-a-go-go-related gene protein degradation by intermittent hypoxia.American journal of physiology. Cell physiology · 2016Article
- 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
- Interaction of Hydrogen Sulfide with Oxygen Sensing under Hypoxia.Oxidative medicine and cellular longevity · 2015Review
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Arterial blood O2 levels are detected by specialized sensory organs called carotid bodies. Voltage-gated Ca(2+) channels (VGCCs) are important for carotid body O2 sensing. Given that T-type VGCCs contribute to nociceptive sensation, we hypothesized that they participate in carotid body O2 sensing. The rat carotid body expresses high levels of mRNA encoding the α1H-subunit, and α1H protein is localized to glomus cells, the primary O2-sensing cells in the chemoreceptor tissue, suggesting that CaV3.2 is the major T-type VGCC isoform expressed in the carotid body. Mibefradil and TTA-A2, selective blockers of the T-type VGCC, markedly attenuated elevation of hypoxia-evoked intracellular Ca(2+) concentration, secretion of catecholamines from glomus cells, and sensory excitation of the rat carotid body. Similar results were obtained in the carotid body and glomus cells from CaV3.2 knockout (Cacna1h(-/-)) mice. Since cystathionine-γ-lyase (CSE)-derived H2S is a critical mediator of the carotid body response to hypoxia, the role of T-type VGCCs in H2S-mediated O2 sensing was examined. Like hypoxia, NaHS, a H2S donor, increased intracellular Ca(2+) concentration and augmented carotid body sensory nerve activity in wild-type mice, and these effects were markedly attenuated in Cacna1h(-/-) mice. In wild-type mice, TTA-A2 markedly attenuated glomus cell and carotid body sensory nerve responses to hypoxia, and these effects were absent in CSE knockout mice. These results demonstrate that CaV3.2 T-type VGCCs contribute to the H2S-mediated carotid body response to hypoxia.
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