scholarly journals Carotid body physiology meets cytochrome c oxidase crystallography Commentary to Ortega-Sáenz P, López-Barneo J. Physiology of the Carotid Body: From Molecules to Disease. Annu Rev Physiol 82: 127–149, 2020. Torres-Torrelo H, Ortega-Sáenz P, Gao L, López-Barneo J. Lactate sensing mechanisms in arterial chemoreceptor cells. Nat Commun 12: 4166, 2021

2022 ◽  
Author(s):  
Helmut Acker ◽  
Joachim Fandrey
Keyword(s):  
Cytochrome C ◽  
Cytochrome C Oxidase ◽  
Carotid Body ◽  
Chemoreceptor Cells ◽  
Arterial Chemoreceptor

Acetylcholine Increases Intracellular Calcium of Arterial Chemoreceptor Cells of Adult Cats

1997 ◽  
Vol 78 (5) ◽  
pp. 2388-2395 ◽  
Author(s):  
Machiko Shirahata ◽  
Robert S. Fitzgerald ◽  
James S. K. Sham
Keyword(s):  
Intracellular Calcium ◽  
Carotid Body ◽  
Calcium Concentration ◽  
Similar Response ◽  
Muscarinic Agonists ◽  
High K ◽  
Chemoreceptor Cells ◽  
Adult Cats ◽  
Kinetics Of ◽  
Arterial Chemoreceptor

Shirahata, Machiko, Robert S. Fitzgerald, and James S. K. Sham. Acetylcholine increases intracellular calcium of arterial chemoreceptor cells of adult cats. J. Neurophysiol. 78: 2388–2395, 1997. Several neurotransmitters have been reported to play important roles in the chemoreception of the carotid body. Among them acetylcholine (ACh) appears to be involved in excitatory processes in the cat carotid body. As one of the steps to elucidate possible roles of ACh in carotid body chemoreception in the cat, we examined the effect of ACh on intracellular calcium concentration ([Ca2+]i) of cultured carotid body cells. The carotid body from adult cats was dissociated and cultured for up to 2 wk. [Ca2+]i was measured from clusters of cells with a microfluorometric technique using Indo-1 AM. Experiments were performed at 37°C, and cells were continuously superfused with modified Krebs solutions equilibrated with 5% CO2-16% O2-79% N2. ACh (100 μM) caused a marked increase in [Ca2+]i in ∼70% of clusters, and the responses to 1–300 μM of ACh were concentration dependent. The magnitude and kinetics of the ACh response were mimicked by the application of nicotine, whereas muscarinic agonists, pilocarpine, and muscarine failed to evoke a similar response. ACh-induced increase in [Ca2+]i was dependent on extracellular Ca2+: it was greatly reduced or completely abolished by a transient removal of extracellular Ca2+. The response was consistently but only partially reduced by caffeine (5 mM) or nifedipine (10 μM). The effect of mecamylamine (100 μM) was inhibitory but small. Moreover, the increase in [Ca2+]i in response to ACh was also observed in some clusters that did not respond to high K (100 mM) Krebs. These results suggest that ACh increases [Ca2+]i of cultured carotid body cells by activating neuronal nicotinic ACh receptors, leading to Ca2+ influx via nicotinic channels. In addition, other pathways such as Ca2+ influx through L-type calcium channels, perhaps secondary to membrane depolarization, and Ca2+ release from intracellular stores may participate in increasing [Ca2+]i in response to ACh. Muscarinic receptors appear to play only a small role, if any.

scholarly journals Genetic basis of oxygen sensing in the carotid body: HIF2α and an isoform switch in cytochrome c oxidase subunit 4

2020 ◽  
Vol 13 (615) ◽  
pp. eaba1302 ◽  
Author(s):  
Tammie Bishop ◽  
Peter J. Ratcliffe
Keyword(s):  
Cytochrome C ◽  
Cytochrome C Oxidase ◽  
Carotid Body ◽  
Genetic Basis ◽  
Hypoxia Inducible Factor ◽  
Oxygen Sensitivity ◽  
Critical Importance ◽  
Glomus Cell ◽  
Oxidase Subunit ◽  
Mechanistic Basis

The mechanistic basis of the marked oxygen sensitivity of glomus cells in the carotid body has long puzzled physiologists. In this issue of Science Signaling, Moreno-Domínguez et al. show the critical importance of high levels of hypoxia-inducible factor, HIF2α/EPAS1, and the nuclear-encoded mitochondrial cytochrome c oxidase subunit, COX4I2, in glomus cell sensitivity to hypoxia.

Sign in / Sign up

Export Citation Format

Share Document