scholarly journals Increase in cytosolic Ca2+produced by hypoxia and other depolarizing stimuli activates a non-selective cation channel in chemoreceptor cells of rat carotid body

2014 ◽  
Vol 592 (9) ◽  
pp. 1975-1992 ◽  
Author(s):  
Dawon Kang ◽  
Jiaju Wang ◽  
James O. Hogan ◽  
Rudi Vennekens ◽  
Marc Freichel ◽  
...  
Keyword(s):  
Carotid Body ◽  
Cation Channel ◽  
Chemoreceptor Cells

Participation of Na+ channels in the response of carotid body chemoreceptor cells to hypoxia

1994 ◽  
Vol 267 (3) ◽  
pp. C738-C744 ◽  
Author(s):  
A. Rocher ◽  
A. Obeso ◽  
M. T. Cachero ◽  
B. Herreros ◽  
C. Gonzalez
Keyword(s):  
Carotid Body ◽  
Neurotransmitter Release ◽  
Marked Reduction ◽  
Adult Rabbit ◽  
Na Channels ◽  
Na Current ◽  
Chemoreceptor Cells ◽  
Cell Depolarization ◽  
First Time ◽  
Mild Hypoxia

The role played by Na+ channels of carotid body (CB) chemoreceptor cells was investigated by studying the effects of tetrodotoxin (TTX) on the release of 3H-labeled catecholamines ([3H]CA) by adult rabbit CBs previously incubated with the precursor [3H]tyrosine. TTX inhibited partially the release of [3H]CA elicited by mild hypoxia (10 or 7% O2) or by depolarizing incubation medium containing 20 or 30 mM KCl, but the response to more intense hypoxia (5 or 2% O2) or to higher KCl concentration (40 or 50 mM) was not significantly affected. The release of [3H]CA elicited by acidic stimuli, either 20% CO2 (pH 6.6) or the protonophore dinitrophenol (100 microM), although comparable in magnitude to that elicited by mild hypoxia, was not modified by TTX. These results provide evidence for the first time that Na+ channels of chemoreceptor cells participate in the transduction of hypoxic stimuli into the neurotransmitter release response of these cells and suggest that Na+ current operates as an amplifying device that enhances the initial cell depolarization mediated by the closure of the O2-sensitive K+ channels. Sympathetic denervation of CBs was followed by a marked reduction in the release of [3H]CA elicited by veratridine or by 20 mM KCl, suggesting that the number of Na+ channels in chemoreceptor cells decreases after denervation.

scholarly journals Coexpression of Galanin and Nestin in the Chemoreceptor Cells of the Human Carotid Body

2015 ◽  
pp. 77-82 ◽  
Author(s):  
Andrea Mazzatenta ◽  
Guya D. Marconi ◽  
Veronica Macchi ◽  
Andrea Porzionato ◽  
Amelia Cataldi ◽  
...  
Keyword(s):  
Carotid Body ◽  
Chemoreceptor Cells ◽  
Human Carotid

scholarly journals Hydroxycobalamin Reveals the Involvement of Hydrogen Sulfide in the Hypoxic Responses of Rat Carotid Body Chemoreceptor Cells

Antioxidants ◽  
2019 ◽  
Vol 8 (3) ◽  
pp. 62
Author(s):  
Teresa Gallego-Martin ◽  
Jesus Prieto-Lloret ◽  
Philip Aaronson ◽  
Asuncion Rocher ◽  
Ana Obeso
Keyword(s):  
Hydrogen Sulfide ◽  
Carotid Body ◽  
Oxygen Sensor ◽  
Catecholamine Release ◽  
Glomus Cells ◽  
Arterial Blood ◽  
Carotid Bodies ◽  
High K ◽  
Chemoreceptor Cells ◽  
Ca2 Channels

Carotid body (CB) chemoreceptor cells sense arterial blood PO2, generating a neurosecretory response proportional to the intensity of hypoxia. Hydrogen sulfide (H2S) is a physiological gaseous messenger that is proposed to act as an oxygen sensor in CBs, although this concept remains controversial. In the present study we have used the H2S scavenger and vitamin B12 analog hydroxycobalamin (Cbl) as a new tool to investigate the involvement of endogenous H2S in CB oxygen sensing. We observed that the slow-release sulfide donor GYY4137 elicited catecholamine release from isolated whole carotid bodies, and that Cbl prevented this response. Cbl also abolished the rise in [Ca2+]i evoked by 50 µM NaHS in enzymatically dispersed CB glomus cells. Moreover, Cbl markedly inhibited the catecholamine release and [Ca2+]i rise caused by hypoxia in isolated CBs and dispersed glomus cells, respectively, whereas it did not alter these responses when they were evoked by high [K+]e. The L-type Ca2+ channel blocker nifedipine slightly inhibited the rise in CB chemoreceptor cells [Ca2+]i elicited by sulfide, whilst causing a somewhat larger attenuation of the hypoxia-induced Ca2+ signal. We conclude that Cbl is a useful and specific tool for studying the function of H2S in cells. Based on its effects on the CB chemoreceptor cells we propose that endogenous H2S is an amplifier of the hypoxic transduction cascade which acts mainly by stimulating non-L-type Ca2+ channels.

scholarly journals Role of Glutathione Redox State in Oxygen Sensing by Carotid Body Chemoreceptor Cells

2004 ◽  
pp. 40-71 ◽  
Author(s):  
Constancio Gonzalez ◽  
Gloria Sanz-Alfayate ◽  
Ana Obeso ◽  
Maria Teresa Agapito
Keyword(s):  
Carotid Body ◽  
Redox State ◽  
Oxygen Sensing ◽  
Chemoreceptor Cells ◽  
Glutathione Redox

Effects of Almitrine Bismesylate on the Ionic Currents of Chemoreceptor Cells from the Carotid Body

1998 ◽  
Vol 53 (2) ◽  
pp. 330-339 ◽  
Author(s):  
J. R. López-López ◽  
M. T. Pérez-García ◽  
E. Canet ◽  
C. Gonzalez
Keyword(s):  
Carotid Body ◽  
Ionic Currents ◽  
Almitrine Bismesylate ◽  
Chemoreceptor Cells

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.

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