scholarly journals EFFECTS OF SINUS NERVE STIMULATION ON CAROTID BODY GLOMUS CELLS

1970 ◽  
Vol 46 (3) ◽  
pp. 544-552 ◽  
Author(s):  
R. D. Yates ◽  
I-Li Chen ◽  
Donald Duncan
Keyword(s):  
Nerve Stimulation ◽  
Carotid Body ◽  
Sympathetic Trunk ◽  
Sympathetic Nerve Stimulation ◽  
Glomus Cells ◽  
Carotid Bodies ◽  
Reserpine Treatment ◽  
Granule Density ◽  
Adult Cats ◽  
Carotid Body Glomus Cells

The sinus nerve or sympathetic trunk was stimulated unilaterally in one group of adult cats or Syrian hamsters while in another group the sinus nerve or sympathetic trunk was cut unilaterally and the animals were given reserpine. In a third group, atropine was administered prior to sinus nerve stimulation. All tissues were processed for the detection of primary monoamines. The carotid bodies on the operated sides were compared with those on the unoperated sides of the same animal in order to determine if amine depletion occurred following the experimental procedures. After sinus nerve stimulation alone, the density of the granules in the glomus cells was decreased, but changes were not noted in the granules following sympathetic nerve stimulation. Sinus nerve stimulation after atropine administration resulted in no change in granule density. Sinus nerve transection followed by reserpine treatment resulted in a greater decrease in granule density on the unoperated than on the operated side. Transection of the sympathetic components to the carotid body followed by reserpine injections resulted in a decrease in granule density in the glomus cells on both the operated and unoperated sides. These results suggest that the sinus nerve must be intact for reserpine to exert an effect and that the sinus nerve may contain efferent fibers which modulate amine secretion.

Fine Structure of Carotid Body: Normal and Anoxic Cats

1967 ◽  
Vol 25 ◽  
pp. 150-151
Author(s):  
Fadhil Al-Lami ◽  
R.G. Murray
Keyword(s):  
Fine Structure ◽  
Adrenal Medulla ◽  
Carotid Body ◽  
Uranyl Acetate ◽  
Lead Citrate ◽  
Glomus Cells ◽  
Sustentacular Cells ◽  
Carotid Bodies

Although the fine structure of the carotid body has been described in several recent reports, uncertainties remain, and the morphological effects of anoxia on the carotid body cells of the cat have never been reported. We have, therefore, studied the fine structure of the carotid body both in normal and severely anoxic cats, and to test the specificity of the effects, have compared them with the effects on adrenal medulla, kidney, and liver of the same animals. Carotid bodies of 50 normal and 15 severely anoxic cats (9% oxygen in nitrogen) were studied. Glutaraldehyde followed by OsO4 fixations, Epon 812 embedding, and uranyl acetate and lead citrate staining, were the technics employed.We have called the two types of glomus cells enclosed and enclosing cells. They correspond to those previously designated as chemoreceptor and sustentacular cells respectively (1). The enclosed cells forming the vast majority, are irregular in shape with many processes and occasional peripheral densities (Fig. 1).

scholarly journals Endogenous H2S is required for hypoxic sensing by carotid body glomus cells

2012 ◽  
Vol 303 (9) ◽  
pp. C916-C923 ◽  
Author(s):  
Vladislav V. Makarenko ◽  
Jayasri Nanduri ◽  
Gayatri Raghuraman ◽  
Aaron P. Fox ◽  
Moataz M. Gadalla ◽  
...  
Keyword(s):  
Carotid Body ◽  
Time Course ◽  
Channel Blocker ◽  
Primary Site ◽  
Dependent Manner ◽  
Free Medium ◽  
Adult Rats ◽  
Glomus Cells ◽  
Dose Dependent ◽  
Carotid Body Glomus Cells

H2S generated by the enzyme cystathionine-γ-lyase (CSE) has been implicated in O2 sensing by the carotid body. The objectives of the present study were to determine whether glomus cells, the primary site of hypoxic sensing in the carotid body, generate H2S in an O2-sensitive manner and whether endogenous H2S is required for O2 sensing by glomus cells. Experiments were performed on glomus cells harvested from anesthetized adult rats as well as age and sex-matched CSE+/+ and CSE−/− mice. Physiological levels of hypoxia (Po2 ∼30 mmHg) increased H2S levels in glomus cells, and dl-propargylglycine (PAG), a CSE inhibitor, prevented this response in a dose-dependent manner. Catecholamine (CA) secretion from glomus cells was monitored by carbon-fiber amperometry. Hypoxia increased CA secretion from rat and mouse glomus cells, and this response was markedly attenuated by PAG and in cells from CSE−/− mice. CA secretion evoked by 40 mM KCl, however, was unaffected by PAG or CSE deletion. Exogenous application of a H2S donor (50 μM NaHS) increased cytosolic Ca2+ concentration ([Ca2+]i) in glomus cells, with a time course and magnitude that are similar to that produced by hypoxia. [Ca2+]i responses to NaHS and hypoxia were markedly attenuated in the presence of Ca2+-free medium or cadmium chloride, a pan voltage-gated Ca2+ channel blocker, or nifedipine, an L-type Ca2+ channel inhibitor, suggesting that both hypoxia and H2S share common Ca2+-activating mechanisms. These results demonstrate that H2S generated by CSE is a physiologic mediator of the glomus cell's response to hypoxia.

Effect of Na+ and K+ channel blockade on baseline and anoxia-induced catecholamine release from rat carotid body

1994 ◽  
Vol 77 (6) ◽  
pp. 2606-2611 ◽  
Author(s):  
T. P. Doyle ◽  
D. F. Donnelly
Keyword(s):  
Carotid Body ◽  
K Channel ◽  
Channel Blockers ◽  
Nerve Activity ◽  
Sham Treatment ◽  
K Channels ◽  
Nerve Response ◽  
Carotid Bodies ◽  
Carotid Body Glomus Cells

Ionic membrane currents are hypothesized to play a major role in determining secretion from carotid body glomus cells, and increased secretion likely mediates the increase in nerve activity in response to hypoxia. The hypothesis that Na+ and K+ channels play an important role in determining secretion and nerve activity was tested by measuring single-fiber afferent nerve activity along with an estimate of free tissue catecholamine using Nafion-covered carbon-fiber micro-electrodes placed in rat carotid bodies in vitro. Baseline and anoxia-stimulated (1 min duration; PO2 of approximately 0 Torr at nadir) levels were quantified. Sham treatment had no significant effect. Tetrodotoxin (2 microns) ablated the nerve activity and reduced peak catecholamine (19.5 +/- 3.1 to 14.5 +/- 3.4 microM; P < 0.05). Cesium (10 microns) had no effect on catecholamine but reduced the nerve response (19.8 +/- 2.7 to 7.8 +/- 2.0 Hz; P < 0.05). 4-Aminopyridine (4 mM) significantly reduced the nerve response (17.2 +/- 3.7 to 4.9 +/- 1.9 Hz; P < 0.05) and increased the baseline (0.9 +/- 0.2 to 3.1 +/- 0.8 microM; P < 0.05) and reduced the peak catecholamine (10.0 to 4.3 +/- 0.8 microM; P < 0.05) levels. These results demonstrate that Na+ and K+ channels play an important role in modulating the secretory and nerve responses. However, channel blockers do not emulate severe hypoxia, suggesting that hypoxia transduction procedes, at least in part, through an alternate pathway.

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 Nitric Oxide Inhibits L-Type Ca2+ Current in Glomus Cells of the Rabbit Carotid Body Via a cGMP-Independent Mechanism

1999 ◽  
Vol 81 (4) ◽  
pp. 1449-1457 ◽  
Author(s):  
Beth A. Summers ◽  
Jeffrey L. Overholt ◽  
Nanduri R. Prabhakar
Keyword(s):  
Nitric Oxide ◽  
Carotid Body ◽  
Channel Blocker ◽  
Adult Rabbit ◽  
Subsequent Formation ◽  
No Donors ◽  
Glomus Cells ◽  
Channel Proteins ◽  
Carotid Bodies ◽  
Independent Mechanism

Nitric oxide inhibits L-type Ca2+ current in glomus cells of the rabbit carotid body via a cGMP-independent mechanism. Previous studies have shown that nitric oxide (NO) inhibits carotid body sensory activity. To begin to understand the cellular mechanisms associated with the actions of NO in the carotid body, we monitored the effects of NO donors on the macroscopic Ca2+ current in glomus cells isolated from rabbit carotid bodies. Experiments were performed on freshly dissociated glomus cells from adult rabbit carotid bodies using the whole cell configuration of the patch-clamp technique. The NO donors sodium nitroprusside (SNP; 600 μM, n = 7) and spermine nitric oxide (SNO; 100 μM, n = 7) inhibited the Ca2+ current in glomus cells in a voltage-independent manner. These effects of NO donors were rapid in onset and peaked within 1 or 2 min. In contrast, the outward K+ current was unaffected by SNP (600 μM, n = 6), indicating that the inhibition by SNP was not a nonspecific membrane effect. 2-(4-carboxyphenyl)-4,4,5,5-tetramethyl-imidazoline-1-oxyl-3-oxide (carboxy-PTIO; 500 μM), an NO scavenger, prevented inhibition of the Ca2+ current by SNP ( n = 7), whereas neither superoxide dismutase (SOD; 2,000 U/ml, n = 4), a superoxide scavenger, nor sodium hydrosulfite (SHS; 1 mM, n = 7), a reducing agent, prevented inhibition of the Ca2+ current by SNP. However, SNP inhibition of the Ca2+ current was reversible in the presence of either SOD or SHS. These results suggest that NO itself inhibits Ca2+current in a reversible manner and that subsequent formation of peroxynitrites results in irreversible inhibition. SNP inhibition of the Ca2+ current was not affected by 30 μM LY 83,583 ( n = 7) nor was it mimicked by 600 μM 8-bromoguanosine 3′:5′-cyclic monophosphate (8-Br-cGMP; n = 6), suggesting that the effects of NO on the Ca2+ current are mediated, in part, via a cGMP-independent mechanism. N-ethylmaleimide (NEM; 2.5 mM, n= 6) prevented the inhibition of the Ca2+ current by SNP, indicating that SNP is acting via a modification of sulfhydryl groups on Ca2+ channel proteins. Norepinephrine (NE; 10 μM) further inhibited the Ca2+ current in the presence of NEM ( n = 7), implying that NEM did not nonspecifically eliminate Ca2+ current modulation. Nisoldipine, an L-type Ca2+ channel blocker (2 μM, n = 6), prevented the inhibition of Ca2+ current by SNP, whereas ω-conotoxin GVIA, an N-type Ca2+ channel blocker (1 μM, n = 9), did not prevent the inhibition of Ca2+ current by SNP. These results demonstrate that NO inhibits L-type Ca2+ channels in adult rabbit glomus cells, in part, due to a modification of calcium channel proteins. The inhibition might provide one plausible mechanism for efferent inhibition of carotid body activity by NO.

Ca2+ Current in Rabbit Carotid Body Glomus Cells Is Conducted by Multiple Types of High-Voltage–Activated Ca2+ Channels

1997 ◽  
Vol 78 (5) ◽  
pp. 2467-2474 ◽  
Author(s):  
Jeffrey L. Overholt ◽  
Nanduri R. Prabhakar
Keyword(s):  
High Voltage ◽  
Carotid Body ◽  
Neurotransmitter Release ◽  
Relative Proportion ◽  
Sensory Transduction ◽  
Arterial Oxygen ◽  
Patch Clamp Technique ◽  
Simultaneous Application ◽  
Glomus Cells ◽  
Carotid Body Glomus Cells

Overholt, Jeffrey L. and Nanduri R. Prabhakar. Ca2+ current in rabbit carotid body glomus cells is conducted by multiple types of high-voltage–activated Ca2+ channels. J. Neurophysiol. 78: 2467–2474, 1997. Carotid bodies are sensory organs that detect changes in arterial oxygen. Glomus cells are presumed to be the initial sites for sensory transduction, and Ca2+-dependent neurotransmitter release from glomus cells is believed to be an obligatory step in this response. Some information exists on the Ca2+ channels in rat glomus cells. However, relatively little is known about the types of Ca2+ channels present in rabbit glomus cells, the species in which most of the neurotransmitter release studies have been performed. Therefore we tested the effect of specific Ca2+ channel blockers on current recorded from freshly dissociated, adult rabbit carotid body glomus cells using the whole cell configuration of the patch-clamp technique. Macroscopic Ba2+ current elicited from a holding potential of −80 mV activated at a V m of approximaely −30 mV, peaked between 0 and +10 mV and did not inactivate during 25-ms steps to positive test potentials. Prolonged (≈2 min) depolarized holding potentials inactivated the current with a V 1/2 of −47 mV. There was no evidence for T-type channels. On steps to 0 mV, 6 mM Co2+ decreased peak inward current by 97 ± 1% (mean ± SE). Nisoldipine (2 μM), 1 μM ω-conotoxin GVIA, and 100 nM ω-agatoxin IVa each blocked a portion of the macroscopic Ca2+ current (30 ± 5, 33 ± 5, and 19 ± 3% after rundown correction, respectively). Simultaneous application of these blockers revealed a resistant current that was not affected by 1 μMω-conotoxin MVIIC. This resistant current constituted 27 ± 5% of the total macroscopic Ca2+ current. Each blocker had an effect in every cell so tested. However, the relative proportion of current blocked varied from cell to cell. These results suggest that L, N, P, and resistant channel types each conduct a significant proportion of the macroscopic Ca2+ current in rabbit glomus cells. Hypoxia-induced neurotransmitter release from glomus cells may involve one or more of these channels.

scholarly journals Hypoxia induces voltage-dependent Ca2+ entry and quantal dopamine secretion in carotid body glomus cells.

1994 ◽  
Vol 91 (21) ◽  
pp. 10208-10211 ◽  
Author(s):  
J. Urena ◽  
R. Fernandez-Chacon ◽  
A. R. Benot ◽  
G. A. Alvarez de Toledo ◽  
J. Lopez-Barneo
Keyword(s):  
Carotid Body ◽  
Glomus Cells ◽  
Voltage Dependent ◽  
Carotid Body Glomus Cells
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