ArticleThe Journal of physiology2003
ATP triggers intracellular Ca2+ release in type II cells of the rat carotid body.
Article in The Journal of physiology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 74 citations in OpenAlex.
- Targeting ecto-5'-nucleotidase (CD73) and cAMP alleviates carotid body hyperactivity and reduces blood pressure in chronically hypoxic rats.The Journal of physiology · 2026Article
- Type II Cells in the Human Carotid Body Display P2X7 Receptor and Pannexin-1 Immunoreactivity.Biomolecules · 2025Article
- Intra-carotid body inter-cellular communication.Journal of the Royal Society of New Zealand · 2023Review
- Neurochemical Anatomy of the Mammalian Carotid Body.Advances in anatomy, embryology, and cell biology · 2023Article
- Mechanisms of Chemosensory Transduction in the Carotid Body.Advances in anatomy, embryology, and cell biology · 2023Article
- Chemoreflex Control as the Cornerstone in Immersion Water Sports: Possible Role on Breath-Hold.Frontiers in physiology · 2022Review
- Carotid body chemoreceptors: physiology, pathology, and implications for health and disease.Physiological reviews · 2021Review
- Neurotransmitter Modulation of Carotid Body Germinal Niche.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
- Expanding Role of Dopaminergic Inhibition in Hypercapnic Responses of Cultured Rat Carotid Body Cells: Involvement of Type II Glial Cells.International journal of molecular sciences · 2020Article
- Molecular Mechanisms of Acute Oxygen Sensing by Arterial Chemoreceptor Cells. Role of Hif2α.Frontiers in physiology · 2020Review
- Adenosine and dopamine oppositely modulate a hyperpolarization-activated current IThe Journal of physiology · 2018Article
- Role of glial-like type II cells as paracrine modulators of carotid body chemoreception.Physiological genomics · 2018Article
- Synaptic Functions of Hemichannels and Pannexons: A Double-Edged Sword.Frontiers in molecular neuroscience · 2018Review
- Sensory Processing and Integration at the Carotid Body Tripartite Synapse: Neurotransmitter Functions and Effects of Chronic Hypoxia.Frontiers in physiology · 2018Review
- Receptor-Receptor Interactions of G Protein-Coupled Receptors in the Carotid Body: A Working Hypothesis.Frontiers in physiology · 2018Article
- Characterization of ectonucleotidase expression in the rat carotid body: regulation by chronic hypoxia.American journal of physiology. Cell physiology · 2017Article
- Evidence that 5-HT stimulates intracellular CaThe Journal of physiology · 2017Article
- Purines and Carotid Body: New Roles in Pathological Conditions.Frontiers in pharmacology · 2017Review
- Purinergic signalling mediates bidirectional crosstalk between chemoreceptor type I and glial-like type II cells of the rat carotid body.The Journal of physiology · 2016Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Using a Ca2+-imaging technique, we studied the action of ATP on the intracellular Ca2+ concentration ([Ca2+]i) of fura-2-loaded mixtures of type I and type II cells dissociated from rat carotid bodies. ATP (100 micro M) triggered a transient rise in [Ca2+]i in the spindle-shaped type II (sustentacular) cells, but not the ovoid type I (glomus) cells. When challenged with ionomycin (1 micro M), no amperometry signal could be detected from the ATP-responsive type II cells, suggesting that these cells lacked catecholamine-containing granules. In contrast, KCl depolarization triggered robust quantal catecholamine release from type I cells that were not responsive to ATP. In type II cells voltage clamped at -70 mV, the ATP-induced [Ca2+]i rise was not accompanied by any current change, suggesting that P2X receptors are not involved. The ATP-induced Ca2+ signal could be observed in the presence of Ni2+ (a blocker of voltage-gated Ca2+ channels) or in the absence of extracellular Ca2+, indicating that Ca2+ release from intracellular stores was the dominant mechanism. The order of purinoreceptor agonist potency in triggering the [Ca2+]i rise was UTP > ATP > 2-methylthioATP >> alpha,beta-methyleneATP, implicating the involvement of P2Y2 receptors. In carotid body sections, immunofluorescence revealed localization of P2Y2 receptors on spindle-shaped type II cells that partially enveloped ovoid type I cells. Since ATP is released from type I cells during hypoxia, we suggest that the ATP-induced Ca2+ signal in type II cells can mediate paracrine interactions within the carotid bodies.
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