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

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 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.

Chronic Caffeine Intake in Adult Rat Inhibits Carotid Body Sensitization Produced by Chronic Sustained Hypoxia but Maintains Intact Chemoreflex Output

2012 ◽  
Vol 82 (6) ◽  
pp. 1056-1065 ◽  
Author(s):  
Silvia V. Conde ◽  
Maria J. Ribeiro ◽  
Ana Obeso ◽  
Ricardo Rigual ◽  
Emilia C. Monteiro ◽  
...  
Keyword(s):  
Carotid Body ◽  
Caffeine Intake ◽  
Adult Rat ◽  
Chronic Caffeine ◽  
Sustained Hypoxia

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

Abstract 202: In Vitro Effect of Trisulfate Disaccharide on ICa (L-type), INa, IK, and the Na/Ca Exchange Current Recorded From Rat Ventricular Myocytes by Patch Clamp

2020 ◽  
Vol 127 (Suppl_1) ◽  
Author(s):  
Enio R Vasques ◽  
Helena Nader ◽  
Ivarne Tersariol ◽  
Godoy Carlos
Keyword(s):  
Patch Clamp ◽  
Intracellular Calcium ◽  
Ventricular Myocytes ◽  
Potassium Currents ◽  
Ionic Currents ◽  
Exchange Current ◽  
Antiarrhythmic Action ◽  
Rat Ventricular Myocytes ◽  
Adult Rat ◽  
Vitro Effect

Background: Ion channels are pharmacological targets for antiarrhythmic action, and drugs currently used for this purpose are generally not specific to a site of action and may act on several channels and even trigger proarrhythmic phenomena. Trisulfate disaccharide (TD) is an heparin fragment known to act on the sodium calcium exchanger (NCX), reducing intracellular calcium in overload situations and reversing arrhytmias, but its action on other ionic currents is unknown. Objective: To evaluate by patch clamp the action of TD at different concentrations in NCX and ionic currents in situations of intracellular calcium overload. Materials and Methods: Adult rat myocytes were obtained from a sample from ventricles. Currents were measured using the whole-cell variant of the patch clamp method. Creation of voltage clamp pulses and data acquisition was controlled by a computer with pClamp software. Peak inward current amplitude was measured for ion currents. For Na/Ca exchange current a ramp voltage protocol was employed. Three different concentrations of Cai (300nM, 400nM and 600nM) were used in separate experiments. One drug concentration was applied per cell (10, 30 and 100 micromolar each). The current sensitive to 5mM nickel was taken as the Na/Ca exchange current. The effects of TD on the INa, L-type Ca, and the potassium currents, transiente outward current (Ito), inwardly rectifying potassium current (IK1), and sustained current (Isus) recorded from adult rat ventricular myocytes were also examined in the same conditions. Results: TD concentration-dependently increased the inward Na/Ca exchange current in all intracellular calcium concentration. The effects of TD on the INa, L-type Ca, and the potassium currents, Ito, IK1 and Isus was associated with less than 30% mean reduction on any current at the highest concentration of TD tested (100 micromolar) and still below the positive block controls for different channels that is above 40% block. Conclusion: TD acts on NCX under different concentrations used, without affecting other ionic currents, suggesting specificity in the mechanism of action and possibly not exerting a pro-arrhythmic activity, this effect being desirable for its possible use in reversal of cardiac arrhythmias.

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.

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