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

scholarly journals Properties of ionic currents from isolated adult rat carotid body chemoreceptor cells: effect of hypoxia.

1997 ◽  
Vol 499 (2) ◽  
pp. 429-441 ◽  
Author(s):  
J R López-López ◽  
C González ◽  
M T Pérez-García
Keyword(s):  
Carotid Body ◽  
Ionic Currents ◽  
Adult Rat ◽  
Chemoreceptor Cells

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.

The Carotid Body and Almitrine Bismesylate

1990 ◽  
pp. 199-206 ◽  
Author(s):  
P. C. G. Nye ◽  
D. L. Maxwell ◽  
P. G. Quirk ◽  
C. Cook
Keyword(s):  
Carotid Body ◽  
Almitrine Bismesylate

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.

Effects of cytochrome P-450 inhibitors on ionic currents in isolated rat type I carotid body cells

1996 ◽  
Vol 271 (1) ◽  
pp. C85-C92 ◽  
Author(s):  
C. J. Hatton ◽  
C. Peers
Keyword(s):  
Carotid Body ◽  
Single Channel ◽  
Ionic Currents ◽  
K Channel ◽  
Type I ◽  
Type I Cells ◽  
Channel Inhibition ◽  
Cytochrome P 450 ◽  
I Cells ◽  
K Currents

Hypoxic chemoreception in the carotid body involves selective inhibition of K+ channels in type I cells. We have investigated whether cytochrome P-450 may act as an O2 sensor coupling hypoxia to K+ channel inhibition, by investigating the actions of P-450 inhibitors to modulate channel activity (recorded using patch-clamp techniques) in type I cells isolated from 8-to 12-day-old rat pups. The imidazole antimycotic P-450 inhibitors miconazole and clotrimazole (1-10 microM) inhibited the Ca(2+)-activated (KCa) and voltage-gated K+ (Kv) currents in isolated type I cells. Single-channel recordings indicated that the KCa channels could be inhibited directly by miconazole. Miconazole also irreversibly inhibited Ca2+ channel currents. By contrast, acute application of the suicide substrate P-450 inhibitor, 1-aminobenzotriazole (1-ABT; 3 mM) was without effect on K+ or Ca2+ currents. Hypoxia (16-23 mmHg) reversibly inhibited K+ currents and prevented the inhibitory actions of miconazole. Furthermore, the inhibitory actions of miconazole could be partially reversed by hypoxia. Pretreatment of cells for 60 min with 3 mM 1-ABT substantially reduced the inhibitory actions of hypoxia on K+ currents. Our results indicate that imidazole antimycotic P-450 inhibitors can directly and nonselectively inhibit ionic channels in type I cells but, more importantly, provide evidence to suggest that hypoxic inhibition of K+ currents in type I cells is mediated in part at least by cytochrome P-450.

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
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