Journal articles: 'Rat carotid body cells'

1

Tse, Amy, Lei Yan, Andy K. Lee, and Frederick W. Tse. "Autocrine and paracrine actions of ATP in rat carotid body." Canadian Journal of Physiology and Pharmacology 90, no. 6 (June 2012): 705–11. http://dx.doi.org/10.1139/y2012-054.

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Carotid bodies are peripheral chemoreceptors that detect lowering of arterial blood O2 level. The carotid body comprises clusters of glomus (type I) cells surrounded by glial-like sustentacular (type II) cells. Hypoxia triggers depolarization and cytosolic [Ca2+] ([Ca2+]i) elevation in glomus cells, resulting in the release of multiple transmitters, including ATP. While ATP has been shown to be an important excitatory transmitter in the stimulation of carotid sinus nerve, there is considerable evidence that ATP exerts autocrine and paracrine actions in carotid body. ATP acting via P2Y1 receptors, causes hyperpolarization in glomus cells and inhibits the hypoxia-mediated [Ca2+]i rise. In contrast, adenosine (an ATP metabolite) triggers depolarization and [Ca2+]i rise in glomus cells via A2A receptors. We suggest that during prolonged hypoxia, the negative and positive feedback actions of ATP and adenosine may result in an oscillatory Ca2+ signal in glomus cells. Such mechanisms may allow cyclic release of transmitters from glomus cells during prolonged hypoxia without causing cellular damage from a persistent [Ca2+]i rise. ATP also stimulates intracellular Ca2+ release in sustentacular cells via P2Y2 receptors. The autocine and paracrine actions of ATP suggest that ATP has important roles in coordinating chemosensory transmission in the carotid body.

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Yamamoto, Y., and K. Taniguchi. "Expression of Tandem P Domain K+ Channel, TREK-1, in the Rat Carotid Body." Journal of Histochemistry & Cytochemistry 54, no. 4 (January 6, 2006): 467–72. http://dx.doi.org/10.1369/jhc.5a6755.2005.

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TREK-1 is one of the important potassium channels for regulating membrane excitability. To examine the distribution of TREK-1 in the rat carotid body, we performed RT-PCR for mRNA expression and in situ hybridization and immunohistochemistry for tissue distribution of TREK-1. RT-PCR detected mRNA expression of TREK-1 in the carotid body. Furthermore, in situ hybridization revealed the localization of TREK-1 mRNA in the glomus cells. TREK-1 immunoreactivity was mainly distributed in the glomus cells and nerve fibers in the carotid body. TREK-1 may modulate potassium current of glomus cells and/or afferent nerve endings in the rat carotid body.

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Pallot, D. J., K. W. Al Neamy, and N. Blakeman. "Quantitative Studies of Rat Carotid Body Type I Cells." Cells Tissues Organs 126, no. 3 (1986): 187–92. http://dx.doi.org/10.1159/000146213.

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Martinez, A., L. Saldise, MJ Ramirez, S. Belzunegui, E. Zudaire, MR Luquin, and F. Cuttitta. "Adrenomedullin expression and function in the rat carotid body." Journal of Endocrinology 176, no. 1 (January 1, 2003): 95–102. http://dx.doi.org/10.1677/joe.0.1760095.

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Adrenomedullin (AM) immunoreactivity has been found in granules of the glomus (type I) cells of the carotid bodies in rats. The identity of these cells was ascertained by colocalization of immunoreactivities for AM and tyrosine hydroxylase in their cytoplasm. Exposure of freshly isolated carotid bodies to synthetic AM resulted in a concentration- and time-dependent degranulation of glomus cells as measured by dopamine (DA) release. DA release reached a zenith 30 min after exposure to AM (94.2% over untreated controls). At this time-point, the response to AM was similar to the one elicited by 5 min of exposure to 100 mM K+. Nevertheless, injection of 1 micro l 60 nM AM/g body weight into the tail vein of the rats did not induce statistical differences in DA release from the carotid bodies. Exposure of the oxygen-sensitive cell line PC-12 to hypoxia elicited an increase in AM mRNA expression and peptide secretion into serum-free conditioned medium. Previous data have shown that elevation of AM expression under hypoxia is mediated through hypoxia-inducible factor-1, and that exposure of chromaffin cells to AM results in degranulation. All these data suggest that AM is an important autocrine regulator of carotid body function.

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Makarenko, Vladislav V., Ying-Jie Peng, Guoxiang Yuan, Aaron P. Fox, Ganesh K. Kumar, Jayasri Nanduri, and Nanduri R. Prabhakar. "CaV3.2 T-type Ca2+ channels in H2S-mediated hypoxic response of the carotid body." American Journal of Physiology-Cell Physiology 308, no. 2 (January 15, 2015): C146—C154. http://dx.doi.org/10.1152/ajpcell.00141.2014.

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Arterial blood O2 levels are detected by specialized sensory organs called carotid bodies. Voltage-gated Ca2+ channels (VGCCs) are important for carotid body O2 sensing. Given that T-type VGCCs contribute to nociceptive sensation, we hypothesized that they participate in carotid body O2 sensing. The rat carotid body expresses high levels of mRNA encoding the α1H-subunit, and α1H protein is localized to glomus cells, the primary O2-sensing cells in the chemoreceptor tissue, suggesting that CaV3.2 is the major T-type VGCC isoform expressed in the carotid body. Mibefradil and TTA-A2, selective blockers of the T-type VGCC, markedly attenuated elevation of hypoxia-evoked intracellular Ca2+ concentration, secretion of catecholamines from glomus cells, and sensory excitation of the rat carotid body. Similar results were obtained in the carotid body and glomus cells from CaV3.2 knockout ( Cacna1h−/−) mice. Since cystathionine-γ-lyase (CSE)-derived H2S is a critical mediator of the carotid body response to hypoxia, the role of T-type VGCCs in H2S-mediated O2 sensing was examined. Like hypoxia, NaHS, a H2S donor, increased intracellular Ca2+ concentration and augmented carotid body sensory nerve activity in wild-type mice, and these effects were markedly attenuated in Cacna1h−/− mice. In wild-type mice, TTA-A2 markedly attenuated glomus cell and carotid body sensory nerve responses to hypoxia, and these effects were absent in CSE knockout mice. These results demonstrate that CaV3.2 T-type VGCCs contribute to the H2S-mediated carotid body response to hypoxia.

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Di Giulio, C., P. G. Data, and S. Lahiri. "Chronic cobalt causes hypertrophy of glomus cells in the rat carotid body." American Journal of Physiology-Cell Physiology 261, no. 1 (July 1, 1991): C102—C105. http://dx.doi.org/10.1152/ajpcell.1991.261.1.c102.

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We tested the hypothesis that chronic cobalt administration would induce carotid body cellular response along with polycythemia as found in chronic hypoxia if common oxygen-sensitive mechanisms were involved in the two instances. Morphometric studies were performed on carotid bodies in male rats that were chronically treated with cobalt chloride (0.17 mumol/kg, ip, daily for 6 wk) and in control rats that received blank saline injections. The rats were anesthetized, blood samples were collected for hematocrit, and the carotid bodies were surgically exposed and were perfused and superfused with the buffered fixative (3% glutaraldehyde plus 1% paraformaldehyde, pH 7.40, 330-340 mosM). The carotid bodies were processed, and ultrathin sections were cut for electron microscopy and morphometry of type I (glomus) and type II cells. Hematocrit increased from 44% in the control to 74% in the cobalt-treated rats, and the mean volume of type I cells increased from 424 to 1,061 microns 3. Type II cells did not show any significant change in size. The results suggest that cobalt stimulated oxygen-sensitive mechanism in the glomus cells of the carotid body and that the glomus cell is a site of oxygen chemosensing.

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Monti-Bloch, L., Vero´nica Abudara, and C. Eyzaguirre. "Electrical communication between glomus cells of the rat carotid body." Brain Research 622, no. 1-2 (September 1993): 119–31. http://dx.doi.org/10.1016/0006-8993(93)90810-a.

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8

Fung, Man-Lung, Siu-Yin Lam, Tung-Po Wong, Yung-Wui Tjong, and Po-Sing Leung. "Carotid Body AT4 Receptor Expression and its Upregulation in Chronic Hypoxia." Open Cardiovascular Medicine Journal 1, no. 1 (June 11, 2007): 1–7. http://dx.doi.org/10.2174/1874192400701010001.

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Hypoxia regulates the local expression of angiotensin-generating system in the rat carotid body and the me-tabolite angiotensin IV (Ang IV) may be involved in the modulation of carotid body function. We tested the hypothesis that Ang IV-binding angiotensin AT4 receptors play a role in the adaptive change of the carotid body in hypoxia. The expression and localization of Ang IV-binding sites and AT4 receptors in the rat carotid bodies were studied with histochemistry. Specific fluorescein-labeled Ang IV binding sites and positive staining of AT4 immunoreactivity were mainly found in lobules in the carotid body. Double-labeling study showed the AT4 receptor was localized in glomus cells containing tyrosine hydroxylase, suggesting the expression in the chemosensitive cells. Intriguingly, the Ang IV-binding and AT4 immunoreactivity were more intense in the carotid body of chronically hypoxic (CH) rats (breathing 10% oxygen for 4 weeks) than the normoxic (Nx) control. Also, the protein level of AT4 receptor was doubled in the CH comparing with the Nx group, supporting an upregulation of the expression in hypoxia. To examine if Ang IV induces intracellular Ca2+ response in the carotid body, cytosolic calcium ([Ca2+]i) was measured by spectrofluorimetry in fura-2-loaded glomus cells dissociated from CH and Nx carotid bodies. Exogenous Ang IV elevated [Ca2+]i in the glomus cells and the Ang IV response was significantly greater in the CH than the Nx group. Hence, hypoxia induces an upregulation of the expression of AT4 receptors in the glomus cells of the carotid body with an increase in the Ang IV-induced [Ca2+]i elevation. This may be an additional pathway enhancing the Ang II action for the activation of chemoreflex in the hypoxic response during chronic hypoxia.

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Otlyga, D. A., O. A. Junemann, E. G. Tsvetkova, K. R. Gorokhov, and S. V. Saveliev. "Immunohistochemical features of the human carotid body." CLINICAL AND EXPERIMENTAL MORPHOLOGY 9, no. 3 (September 23, 2020): 61–67. http://dx.doi.org/10.31088/cem2020.9.3.61-67.

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Introduction. The carotid body is a chemoreceptor organ and the initial link of the reflex regulation of car-diovascular and respiratory systems. However, molecular genetic and immunohistochemical characteristics of the human carotid body remains underinvestigated. Although there are numerous studies of the second half of the 20th century devoted to the classical light-optical histology of the human organ, the immunohis-tochemical investigations are very few. The aim of our study was to clarify immunohistochemical features of the human carotid body in comparison with those of the most commonly used laboratory animals. Materials and methods. The study was performed on 10 carotid bodies of the adult human of different ages of both sexes using immunoperoxidase labeling with antibodies to bIII-tubulin, tyrosine hydroxylase, syn-aptophysin, PGP9.5, neurofilaments 200kDa, S100, and GFAP. Results. Nerve fibers passing between the lobules, as well as entering them, were positive for bIII-tubulin, tyrosine hydroxylase, PGP9.5 and neurofilaments. Type I cells had cytoplasmic reaction for bIII-tubulin and synaptophysin as well as cytoplasmic and nuclear staining for PGP9.5. At the same time, they had weaker reaction for tyrosine hydroxylase. Type II cells were positive for GFAP and S100. Conclusion. Immunohistochemical characteristics of the human carotid body were similar to those of rats and mice. The human carotid body cells and nerve fibers showed the same distribution of PGP9.5, bIII-tubulin, synaptophysin, neurofilaments, GFAP and S100 as rat and mouse carotid body cells. However, human carotid body reaction for tyrosine hydroxylase was much lower, which may indicate a smaller amount of synthesized catecholamines compared to the carotid body in rats and mice. Keywords: human carotid body, immunohistochemistry, sympathoadrenal system, tyrosine hydroxylase

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Stea, A., and C. A. Nurse. "Chloride channels in cultured glomus cells of the rat carotid body." American Journal of Physiology-Cell Physiology 257, no. 2 (August 1, 1989): C174—C181. http://dx.doi.org/10.1152/ajpcell.1989.257.2.c174.

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As part of our investigations on the chemosensory mechanisms in the rat carotid body, we are studying the physiology of the parenchymal glomus cells by the patch-clamp technique. Here we characterize a large-conductance chloride channel (approximately 296 pS) with random open and closed kinetics in inside-out patches of cultured glomus cells. The open-state probability (Po; mean = 0.61) was hardly affected by membrane potential (-50 to +50 mV) and cytoplasmic calcium (0-1 mM). Similarly, the channel did not appear to be regulated by cytoplasmic nucleotides (1 mM) or pH (6.5-8). Ion-substitution experiments yielded the following selectivity sequence: chloride greater than bicarbonate greater than sulfate greater than glutamate approximately sodium. Single-channel currents were reversibly reduced or blocked by anthracene-9-carboxylic acid (5-10 mM) but were unaffected by stilbene derivatives (0.5-1 mM), by furosemide (1 mM), and by 5-nitro-2-(3-phenyl-propylamino)benzoic acid (0.01 mM). Because these cultured glomus cells have been shown to express carbonic anhydrase, it is inferred that the chloride channels may play an important role in the physiology of glomus cells by aiding in the regulation of pHi and the resting potential via bicarbonate and chloride permeability.

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11

Donnelly, D. F., and D. Kholwadwala. "Hypoxia decreases intracellular calcium in adult rat carotid body glomus cells." Journal of Neurophysiology 67, no. 6 (June 1, 1992): 1543–51. http://dx.doi.org/10.1152/jn.1992.67.6.1543.

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1. Carotid body chemoreceptors were removed intact from adult rats and subjected to protease and collagenase enzymatic digestion of connective tissue. 2. Recordings from the sinus nerve demonstrated that chemotransduction remains intact for at least 2-3 h after isolation, enzyme exposure, and suspension in N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid (HEPES)-buffered saline at room PO2. 3. After mechanical dissociation, the interrelationship between changes in extracellular PO2 and pH and relative changes in intracellular calcium (Ca2+i) were observed in glomus cells with the use of fluo-3 and confocal microscopy. 4. Brief (60-s) decreases in PO2 from 150 mmHg to near 0 mmHg, at nadir, caused a marked reduction in Ca2+i (peak delta F/F0 = -32 +/- 3%, mean +/- SE, n = 43), which rapidly recovered after reoxygenation. The decrease was reproducible from trial to trial and was also observed in HCO3(-)-buffered Ringer solution. 5. Superfusion with Ca(2+)-free HEPES saline with 1 mM ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA) blocked the hypoxia-induced increase in afferent chemoreceptor activity in vitro. Superfusion of the same solution over isolated cells for 15 min caused a large decrease in Ca2+i (-34 +/- 7%, n = 16). 6. In the presence of Ca(2+)-free HEPES, reoxygenation caused calcium fluorescence to increase. This suggests that the Ca2+ decrease during hypoxia is due, at least partially, to binding to an intracellular site. 7. Extracellular cobalt (1 mM, 15 min) also reversibly blocked the chemoreceptor response to hypoxia, in vitro, and caused a reduction in Ca2+i (delta F/F0 = -37 +/- 8%, n = 11).(ABSTRACT TRUNCATED AT 250 WORDS)

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Carpenter, Elisabeth, and Chris Peers. "A standing Na+ conductance in rat carotid body type I cells." Neuroreport 12, no. 7 (May 2001): 1421–25. http://dx.doi.org/10.1097/00001756-200105250-00025.

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Wang, Xi, Bai-Ren Wang, Xiao-Li Duan, Ping Zhang, Yu-Qiang Ding, Yi Jia, Xi-Ying Jiao, and Gong Ju. "Strong Expression of Interleukin-1 Receptor Type I in the Rat Carotid Body." Journal of Histochemistry & Cytochemistry 50, no. 12 (December 2002): 1677–84. http://dx.doi.org/10.1177/002215540205001213.

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One of the unsolved key questions in neuroimmunomodulation is how peripheral immune signals are transmitted to the brain. It has been reported that the vagus might play a role in this regard. The underlying mechanism for this immune system-to-brain communication route is related to the binding of cytokines, such as interleukin (IL)-1β originating from activated immune cells, to their receptors in glomus cells of the vagal paraganglia. The existence of IL-1 receptor type I (IL-1RI) in vagal paraganglia has been proved. On the basis of these studies, a hypothesis is raised that the carotid body, as the largest paraganglion, might play a similar role to that of its abdominal partner. In this study we examined the distribution of IL-1RI in the carotid body by immunohistochemistry (IHC) and Western blotting techniques. The IHC results showed that almost all glomus cells in the carotid body displayed strong IL-1RI immunoreactivity. The IL-1RI-immunoreactive products were localized in the cytoplasm, nucleus, and cell membrane of the glomus cells. The Western blotting results also confirmed the existence of IL-1RI in both membranous and cytoplasmic elements of the carotid body. These results imply that the carotid body not only serves as a chemoreceptor for modulation of cardiorespiratory performance, as traditionally recognized, but also acts as a cytokine chemorereceptor for sensing immune signals.

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He, L., B. Dinger, and S. Fidone. "Effect of chronic hypoxia on cholinergic chemotransmission in rat carotid body." Journal of Applied Physiology 98, no. 2 (February 2005): 614–19. http://dx.doi.org/10.1152/japplphysiol.00714.2004.

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Current views suggest that oxygen sensing in the carotid body occurs in chemosensory type I cells, which excite synaptically apposed chemoafferent nerve terminals in the carotid sinus nerve (CSN). Prolonged exposure in a low-oxygen environment [i.e., chronic hypoxia (CH)] elicits an elevated stimulus-evoked discharge in chemoreceptor CSN fibers (i.e., increased chemosensitivity). In the present study, we evaluated cholinergic chemotransmission in the rat carotid body in an effort to test the hypothesis that CH enhances ACh-mediated synaptic activity between type I cells and chemoafferent nerve terminals. Animals were exposed in a hypobaric chamber (barometric pressure = 380 Torr) for 9–22 days before evaluation of chemoreceptor activity using an in vitro carotid body/CSN preparation. Nerve activity evoked by ACh was significantly larger ( P < 0.01) after CH, suggesting increased expression of cholinergic receptors. Approximately 80% of the CSN impulse activity elicited by ACh (100- or 1,000-μg bolus) in both normal and CH preparations was blocked by the specific nicotinic receptor antagonist mecamylamine (100 μM). CSN activity elicited by acute hypoxia or hypercapnia in normal preparations was likewise blocked (≥80%) in the presence of 100 μM mecamylamine, but after CH the enhanced CSN activity elicited by acute hypoxia or hypercapnia was not reduced in the presence of 100 or 500 μM mecamylamine. A muscarinic receptor antagonist, atropine (10 μM), and a specific nicotinic receptor α7 subunit antagonist, methyllycaconatine (50 nM), blocked ∼50% of the hypoxia-evoked activity in normal preparations but were ineffective after CH. Prolonged exposure to hypoxia appears to dramatically alter chemotransmission in the carotid body, and may induce alternative neurotransmitter mechanisms and/or electrical coupling between type I cells and chemoafferent nerve terminals.

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He, L., J. Chen, B. Dinger, L. Stensaas, and S. Fidone. "Effect of chronic hypoxia on purinergic synaptic transmission in rat carotid body." Journal of Applied Physiology 100, no. 1 (January 2006): 157–62. http://dx.doi.org/10.1152/japplphysiol.00859.2005.

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Recent studies indicate that chemoafferent nerve fiber excitation in the rat carotid body is mediated by acetylcholine and ATP, acting at nicotinic cholinergic receptors and P2X2 purinoceptors, respectively. We previously demonstrated that, after a 10- to 14-day exposure to chronic hypoxia (CH), the nicotinic cholinergic receptor blocker mecamylamine no longer inhibits rat carotid sinus nerve (CSN) activity evoked by an acute hypoxic challenge. The present experiments examined the effects of CH (9–16 days at 380 Torr) on the expression of P2X2 purinoceptors in carotid body and chemoafferent neurons, as well as the effectiveness of P2X2 receptor blocking drugs on CSN activity evoked by hypoxia. In the normal carotid body, immunocytochemical studies demonstrated a dense plexus of P2X2-positive nerve fibers penetrating lobules of type I cells. In addition, type I cells were lightly stained, indicating P2X2 receptor expression. After CH, the intensity of P2X2 receptor immunostaining was maintained in chemosensory type I cells and in the soma of chemoafferent neurons. P2 receptor expression on type I cells was confirmed by demonstrations of ATP-evoked increased intracellular Ca2+; this response was modulated by simultaneous exposure to hypoxia. In normal preparations, CSN activity evoked by hypoxia in vitro was 65% inhibited in the presence of specific P2X2 receptor antagonists. However, unlike the absence of mecamylamine action after CH, P2X2 antagonists remained effective against hypoxia-evoked activity after CH. Our findings indicate that ATP acting at P2X2 receptors contributes to adjusted chemoreceptor activity after CH, indicating a possible role for purinergic mechanisms in the adaptation of the carotid body in a chronic low-O2 environment.

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Chen, J., L. He, B. Dinger, L. Stensaas, and S. Fidone. "Chronic hypoxia upregulates connexin43 expression in rat carotid body and petrosal ganglion." Journal of Applied Physiology 92, no. 4 (April 1, 2002): 1480–86. http://dx.doi.org/10.1152/japplphysiol.00077.2001.

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Recent studies have demonstrated that oxygen-sensitive type I cells in the carotid body express the gap junction-forming protein connexin43 (Cx43). In the present study, we examined the hypothesis that chronic exposure to hypoxia increases Cx43 expression in type I cells as well as in chemoafferent neurons in the petrosal ganglion. Immunocytochemical studies in tissues from normal rats revealed diffuse and granular Cx43-like immunoreactivity in the cytoplasm of type I cells and dense punctate spots of immunoreactive product at the margins of type I cells and near the borders of chemosensory cell lobules. Cx43-like immunoreactivity was not detectable in petrosal ganglion neurons from normal animals. After a 2-wk exposure to hypobaric (380 Torr) hypoxia, Cx43 immunostaining was substantially enhanced in and around type I cells. Moreover, chronic hypoxia elicited the expression of Cx43-like immunoreactivity in the cytoplasm of afferent neurons throughout the petrosal ganglion. Quantitative RT-PCR studies indicate that chronic hypoxia evokes a substantial increase in Cx43 mRNA levels in the carotid body, along with a marked elevation of Cx43 expression in the petrosal ganglion. Increased Cx43 expression and gap junction formation in type I cells and sensory neurons may contribute to carotid body adaptation during sustained stimulation in extreme physiological conditions.

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Bamford, Owen S., Laura M. Sterni, Michael J. Wasicko, Marshall H. Montrose, and John L. Carroll. "Postnatal maturation of carotid body and type I cell chemoreception in the rat." American Journal of Physiology-Lung Cellular and Molecular Physiology 276, no. 5 (May 1, 1999): L875—L884. http://dx.doi.org/10.1152/ajplung.1999.276.5.l875.

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The site of postnatal maturation of carotid body chemoreception is unclear. To test the hypothesis that maturation occurs synchronously in type I cells and the whole carotid body, the development of changes in the intracellular Ca2+ concentration responses to hypoxia, CO2, and combined challenges was studied with fluorescence microscopy in type I cells and compared with the development of carotid sinus nerve (CSN) responses recorded in vitro from term fetal to 3-wk animals. Type I cell responses to all challenges increased between 1 and 8 days and then remained constant, with no multiplicative O2-CO2interaction at any age. The CSN response to hypoxia also matured by 8 days, but CSN responses to CO2 did not change significantly with age. Multiplicative O2-CO2interaction occurred in the CSN response at 2–3 wk but not in younger groups. We conclude that type I cell maturation underlies maturation of the CSN response to hypoxia. However, because development of responses to CO2 and combined hypoxia-CO2 challenges differed between type I cells and the CSN, responses to these stimuli must mature at other, unidentified sites within the developing carotid body.

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Kobayashi, Shuichi, Laura Conforti, and David E. Millhorn. "Gene expression and function of adenosine A2A receptor in the rat carotid body." American Journal of Physiology-Lung Cellular and Molecular Physiology 279, no. 2 (August 1, 2000): L273—L282. http://dx.doi.org/10.1152/ajplung.2000.279.2.l273.

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The present study was undertaken to determine whether rat carotid bodies express adenosine (Ado) A2A receptors and whether this receptor is involved in the cellular response to hypoxia. Our results demonstrate that rat carotid bodies express the A2A and A2B Ado receptor mRNAs but not the A1 or A3 receptor mRNAs as determined by reverse transcriptase-polymerase chain reaction. In situ hybridization confirmed the expression of the A2A receptor mRNA. Immunohistochemical studies further showed that the A2A receptor is expressed in the carotid body and that it is colocalized with tyrosine hydroxylase in type I cells. Whole cell voltage-clamp studies using isolated type I cells showed that Ado inhibited the voltage-dependent Ca2+ currents and that this inhibition was abolished by the selective A2A receptor antagonist ZM-241385. Ca2+ imaging studies using fura 2 revealed that exposure to severe hypoxia induced elevation of intracellular Ca2+ concentration ([Ca2+]i) in type I cells and that extracellularly applied Ado significantly attenuated the hypoxia-induced elevation of [Ca2+]i. Taken together, our findings indicate that A2A receptors are present in type I cells and that activation of A2Areceptors modulates Ca2+ accumulation during hypoxia. This mechanism may play a role in regulating intracellular Ca2+homeostasis and cellular excitability during hypoxia.

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H�hler, Brigitte, Bernd Mayer, and Wolfgang Kummer. "Nitric oxide synthase in the rat carotid body and carotid sinus." Cell and Tissue Research 276, no. 3 (June 1, 1994): 559–64. http://dx.doi.org/10.1007/s004410050118.

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Fieber, L. A., and E. W. McCleskey. "L-type calcium channels in type I cells of the rat carotid body." Journal of Neurophysiology 70, no. 4 (October 1, 1993): 1378–84. http://dx.doi.org/10.1152/jn.1993.70.4.1378.

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1. Whole-cell and cell-attached patch-clamp recordings were made from enzymatically isolated type I cells from the carotid body of adult rats. Voltage-dependent K+ and Ca2+ channels were observed, but there was no detectable Na+ current. In this respect, rat carotid body cells are unlike those from rabbit, which have Na+ currents and Na(+)-dependent action potentials. 2. The observed Ca2+ channels had the following properties: 1) activation requires voltage steps above -20 mV; 2) little inactivation occurred with holding voltages below -40 mV; 3) one single-channel conductance of 21 pS was found with 90 or 110 mM Ba2+ in the cell-attached pipette and this was the only conductance observed; 4) open probability was increased by the dihydropyridine Ca2+ channel agonist Bay K 8644 and was decreased by the antagonist nifedipine; and 5) omega-conotoxin had little or no effect on the channels. These are properties expected of L-type Ca2+ channels. 3. To investigate whether these voltage-dependent channels would be available for opening on membrane depolarization, we measured the type I cell resting membrane potential noninvasively using unitary openings of the L-type Ca2+ channel with Bay K 8644 in the cell-attached pipette. Resting potentials ranged from -62 to -13 mV, with a mean of -32 mV in 12 cells. 4. Judging from single-channel conductance and pharmacology, the Ca2+ current is mostly, if not solely, carried by L channels. Thus it should be possible to use modulators of L channel activity to determine the role of Ca2+ channels in stimulus-secretion coupling in the rat carotid body.

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Koerner, Pia, Christian Hesslinger, Agnes Schaefermeyer, Christian Prinz, and Manfred Gratzl. "Evidence for histamine as a transmitter in rat carotid body sensor cells." Journal of Neurochemistry 91, no. 2 (October 2004): 493–500. http://dx.doi.org/10.1111/j.1471-4159.2004.02740.x.

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Gauda, Estelle B., Reed Cooper, Shereé M. Johnson, Gabrielle L. McLemore, and Cathleen Marshall. "Autonomic microganglion cells: a source of acetylcholine in the rat carotid body." Journal of Applied Physiology 96, no. 1 (January 2004): 384–91. http://dx.doi.org/10.1152/japplphysiol.00897.2003.

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Hypoxic chemosensitivity of peripheral arterial chemoreceptors and the ventilatory response to O2 deprivation increases with postnatal development. Multiple putative neurotransmitters, which are synthesized in the carotid body (CB), are thought to mediate signals generated by hypoxia. Acetylcholine (ACh) is believed to be a major excitatory neurotransmitter participating in hypoxic chemosensitivity. However, it is not known whether ACh originates from type I cells in the CB. In these studies, we tested the hypothesis that choline acetyltransferase (ChAT) and vesicular ACh transporter (VAChT) mRNAs are expressed in the CB and that mRNA levels would increase with postnatal maturation or exposure to hypoxia. Semiquantitative in situ hybridization histochemistry and immunohistochemistry were used to localize cholinergic markers within neurons and cells of the rat CB, the nodose-petrosal-jugular ganglion complex, and the superior cervical ganglion up to postnatal day 28. We show that the pattern of distribution, in tissue sections, is similar for both ACh markers; however, the level of VAChT mRNA is uniformly greater than that of ChAT. VAChT mRNA and immunoreactivity are detected abundantly in the nodose-petrosal-jugular ganglion complex in a number of microganglion cells embedded in nerve fibers innervating the CB for all postnatal groups, whereas ChAT mRNA is detected in only a few of these cells. Contrary to our hypothesis, postnatal maturation caused a reduction in ACh trait expression, whereas hypoxic exposure did not induce the upregulation of VAChT and ChAT mRNA levels in the CB, microganglion, or within the ganglion complex. The present findings indicate that the source of ACh in the CB is likely within autonomic microganglion cells and cholinergic nerve terminals.

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Ortega-Saenz, P., R. Pardal, M. Garcia-Fernandez, and J. Lopez-Barneo. "Rotenone selectively occludes sensitivity to hypoxia in rat carotid body glomus cells." Journal of Physiology 548, no. 3 (March 7, 2003): 789–800. http://dx.doi.org/10.1113/jphysiol.2003.039693.

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Agapito, Maria Teresa, Gloria Sanz-Alfayate, Angela Gomez-Niño, Constancio Gonzalez, and Ana Obeso. "General redox environment and carotid body chemoreceptor function." American Journal of Physiology-Cell Physiology 296, no. 3 (March 2009): C620—C631. http://dx.doi.org/10.1152/ajpcell.00542.2008.

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Carotid body (CB) chemoreceptor cells detect physiological levels of hypoxia and generate a hyperventilation, homeostatic in nature, aimed to minimize the deleterious effects of hypoxia. Intimate mechanisms involved in oxygen sensing in chemoreceptor cells remain largely unknown, but reactive oxygen species (ROS) had been proposed as mediators of this process. We have determined glutathione levels and calculated glutathione redox potential ( EGSH; indicator of the general redox environment of cells) in rat diaphragms incubated in the presence of oxidizing agents of two types: nonpermeating and permeating through cell membranes; in the latter group, unspecific oxidants and inhibitors of ROS-disposing enzymes were used. Selected concentrations of oxidizing agents were tested for their ability to modify the normoxic and hypoxic activity of chemoreceptor cells measured in vitro as their rate of release of neurotransmitters. Results evidence variable relationships between EGSHand the activity of chemoreceptor cells. The independence of chemoreceptor cell activity from the EGSHwould imply that the ability of the CB to play its homeostatic role is largely preserved in any pathological or toxicological contingency causing oxidative stress. Consistent with this suggestion, it was also found that CB-mediated hypoxic hyperventilation was not altered by treatment of intact animals with agents that markedly decreased the EGSHin all tissues assayed.

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Gomez-Niño, Angela, Ana Obeso, Jose Antonio Baranda, Jaime Santo-Domingo, Jose Ramon Lopez-Lopez, and Constancio Gonzalez. "MaxiK potassium channels in the function of chemoreceptor cells of the rat carotid body." American Journal of Physiology-Cell Physiology 297, no. 3 (September 2009): C715—C722. http://dx.doi.org/10.1152/ajpcell.00507.2008.

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Hypoxia activates chemoreceptor cells of the carotid body (CB) promoting an increase in their normoxic release of neurotransmitters. Catecholamine (CA) release rate parallels the intensity of hypoxia. Coupling of hypoxia to CA release requires cell depolarization, produced by inhibition of O2-regulated K+ channels, and Ca2+ entering the cells via voltage-operated channels. In rat chemoreceptor cells hypoxia inhibits large-conductance, calcium-sensitive K channels (maxiK) and a two-pore domain weakly inward rectifying K+ channel (TWIK)-like acid-sensitive K+ channel (TASK)-like channel, but the significance of maxiK is controversial. A proposal envisions maxiK contributing to set the membrane potential ( Em) and the hypoxic response, but the proposal is denied by authors finding that maxiK inhibition does not depolarize chemoreceptor cells or alters intracellular Ca2+ concentration or CA release in normoxia or hypoxia. We found that maxiK channel blockers (tetraethylammonium and iberiotoxin) did not modify CA release in rat chemoreceptor cells, in either normoxia or hypoxia, and iberiotoxin did not alter the Ca2+ transients elicited by hypoxia. On the contrary, both maxiK blockers increased the responses elicited by dinitrophenol, a stimulus we demonstrate does not affect maxiK channels in isolated patches of rat chemoreceptor cells. We conclude that in rat chemoreceptor cells maxiK channels do not contribute to the genesis of the Em, and that their full inhibition by hypoxia, preclude further inhibition by maxiK channel blockers. We suggest that full inhibition of this channel is required to generate the spiking behavior of the cells in acute hypoxia.

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M-L, Fung, SY Lam, X. Dong, Y. Chen, and PS Leung. "Postnatal hypoxemia increases angiotensin II sensitivity and up-regulates AT1a angiotensin receptors in rat carotid body chemoreceptors." Journal of Endocrinology 173, no. 2 (May 1, 2002): 305–13. http://dx.doi.org/10.1677/joe.0.1730305.

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In the present study, the effects of postnatal hypoxemia on the AT1 angiotensin receptor-mediated activities in the rat carotid body were studied. Angiotensin II (Ang II) concentration-dependently increased the chemoreceptor afferent activity in the isolated carotid body. Single- or pauci-fiber recording of the sinus nerve revealed that the afferent response to Ang II was enhanced in the postnatally hypoxic carotid body. To determine whether the increased sensitivity to Ang II is mediated by changes in the functional expression of Ang II receptors in the carotid body chemoreceptors, cytosolic calcium ([Ca2+]i) was measured by spectrofluorimetry in fura-2 acetoxymethyl ester-loaded type I cells dissociated from carotid bodies. Ang II (25-100 nM) concentration-dependently increased [Ca2+]i in the type I cells. The proportion of clusters of type I cells responsive to Ang II was higher in the postnatally hypoxic group than in the normoxic control (89 vs 66%). In addition, the peak [Ca2+]i response to Ang II was enhanced 2- to 3-fold in the postnatally hypoxic group. The [Ca2+]i response to Ang II was abolished by pretreatment with losartan (1 microM), an AT1 receptor antagonist, but not by PD-123177 (1 microM), an AT(2) antagonist. Double-labeling immunohistochemistry confirmed that an enhanced immunoreactivity for AT1 receptor was co-localized to the lobules of type I cells in the hypoxic group. In addition, RT-PCR analysis of subtypes of AT1 receptors showed an up-regulation of AT1a but a down-regulation of AT1b receptors, indicating a differential regulation of the expression of AT1 receptor subtypes by postnatal hypoxia in the carotid body. These data suggest that postnatal hypoxemia is associated with an increased sensitivity of peripheral chemoreceptors in response to Ang II and an up-regulation of AT1a receptor-mediated [Ca2+]i activity of the chemoreceptors. This modulation may be important for adaptation of carotid body functions in the hypoxic ventilatory response and in electrolyte and water homeostasis during perinatal and postnatal hypoxia.

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He, L., X. Liu, J. Chen, B. Dinger, L. Stensaas, and S. Fidone. "Modulation of chronic hypoxia-induced chemoreceptor hypersensitivity by NADPH oxidase subunits in rat carotid body." Journal of Applied Physiology 108, no. 5 (May 2010): 1304–10. http://dx.doi.org/10.1152/japplphysiol.00766.2009.

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Previous studies in our laboratory established that reactive oxygen species (ROS) generated by NADPH oxidase (NOX) facilitate the open state of a subset of K+ channels in oxygen-sensitive type I cells of the carotid body. Thus pharmacological inhibition of NOX or deletion of a NOX gene resulted in enhanced chemoreceptor sensitivity to hypoxia. The present study tests the hypothesis that chronic hypoxia (CH)-induced hypersensitivity of chemoreceptors is modulated by increased NOX activity and elevated levels of ROS. Measurements of dihydroethidium fluorescence in carotid body tissue slices showed that increased ROS production following CH (14 days, 380 Torr) was blocked by the specific NOX inhibitor 4-(2-amino-ethyl)benzenesulfonyl fluoride (AEBSF, 3 μM). Consistent with these findings, in normal carotid body AEBSF elicited a small increase in the chemoreceptor nerve discharge evoked by an acute hypoxic challenge, whereas after 9 days of CH the effect of the NOX inhibitor was some threefold larger ( P < 0.001). Evaluation of gene expression after 7 days of CH showed increases in the isoforms NOX2 (∼1.5-fold) and NOX4 (∼3.8-fold) and also increased presence of the regulatory subunit p47phox (∼4.2-fold). Involvement of p47phox was further implicated in studies of isolated type I cells that demonstrated an ∼8-fold and an ∼11-fold increase in mRNA after 1 and 3 days, respectively, of hypoxia in vivo. These findings were confirmed in immunocytochemical studies of carotid body tissue that showed a robust increase of p47phox in type I cells after 14 days of CH. Our findings suggest that increased ROS production by NOX enzymes in type I cells dampens CH-induced hypersensitivity in carotid body chemoreceptors.

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Leung, PS, SY Lam, and ML Fung. "Chronic hypoxia upregulates the expression and function of AT(1) receptor in rat carotid body." Journal of Endocrinology 167, no. 3 (December 1, 2000): 517–24. http://dx.doi.org/10.1677/joe.0.1670517.

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In the present study, the effects of chronic hypoxia on the expression and localization of angiotensin II (Ang II) receptors are investigated by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) and by immunohistochemistry. The effect of chronic hypoxia on the carotid body chemoreceptor activity was also examined by in vitro electrophysiology. Results from RT-PCR revealed that chronic hypoxia exhibited differential effects on the gene expression of Ang II receptors, namely AT(1) and AT(2), in the carotid body. The mRNA expression for subtypes of the AT(1) receptor, AT(1a) and AT(1b), was significantly increased in the carotid body with chronic hypoxia. To further investigate the localization of the AT(1) receptor, an immunohistochemical study was performed. The results showed that AT(1) receptor immunoreactivity was found in lobules of glomus cells in the carotid body and the immunoreactivity was more intense in chronic hypoxia than in normoxic controls. In vitro electrophysiological studies consistently demonstrated that chronic hypoxia enhanced the AT(1) receptor-mediated excitation of carotid body chemoreceptor activity. These data suggest that chronic hypoxia upregulates the transcriptional and post-transcriptional expression of AT(1) receptors in the rat carotid body. The upregulation of the expression also enhances AT(1) receptor-mediated excitation of the carotid body afferent activity. This might be important in the modulation of cardiorespiratory functions as well as fluid and electrolyte homeostasis during chronic hypoxia.

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Kim, Donghee, James O. Hogan, and Carl White. "Ca2+ oscillations in rat carotid body type 1 cells in normoxia and hypoxia." American Journal of Physiology-Cell Physiology 318, no. 2 (February 1, 2020): C430—C438. http://dx.doi.org/10.1152/ajpcell.00442.2019.

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We studied the mechanisms by which carotid body glomus (type 1) cells produce spontaneous Ca2+ oscillations in normoxia and hypoxia. In cells perfused with normoxic solution at 37°C, we observed relatively uniform, low-frequency Ca2+ oscillations in >60% of cells, with each cell showing its own intrinsic frequency and amplitude. The mean frequency and amplitude of Ca2+ oscillations were 0.6 ± 0.1 Hz and 180 ± 42 nM, respectively. The duration of each Ca2+ oscillation ranged from 14 to 26 s (mean of ∼20 s). Inhibition of inositol (1,4,5)-trisphosphate receptor and store-operated Ca2+ entry (SOCE) using 2-APB abolished Ca2+ oscillations. Inhibition of endoplasmic reticulum Ca2+-ATPase (SERCA) using thapsigargin abolished Ca2+ oscillations. ML-9, an inhibitor of STIM1 translocation, also strongly reduced Ca2+ oscillations. Inhibitors of L- and T-type Ca2+ channels (Cav; verapamil>nifedipine>TTA-P2) markedly reduced the frequency of Ca2+ oscillations. Thus, Ca2+ oscillations observed in normoxia were caused by cyclical Ca2+ fluxes at the ER, which was supported by Ca2+ influx via Ca2+ channels. Hypoxia (2–5% O2) increased the frequency and amplitude of Ca2+ oscillations, and Cav inhibitors (verapamil>nifedipine>>TTA-P2) reduced these effects of hypoxia. Our study shows that Ca2+ oscillations represent the basic Ca2+ signaling mechanism in normoxia and hypoxia in CB glomus cells.

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Burlon, Drew C., Heidi L. Jordan, and Christopher N. Wyatt. "Presynaptic regulation of isolated neonatal rat carotid body type I cells by histamine." Respiratory Physiology & Neurobiology 168, no. 3 (September 2009): 218–23. http://dx.doi.org/10.1016/j.resp.2009.07.002.

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31

Kim, Donghee, Insook Kim, Justin R. Papreck, David F. Donnelly, and John L. Carroll. "Characterization of an ATP-sensitive K+ channel in rat carotid body glomus cells." Respiratory Physiology & Neurobiology 177, no. 3 (August 2011): 247–55. http://dx.doi.org/10.1016/j.resp.2011.04.015.

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32

Kim, Insook, Dongjin Yang, John L. Carroll, and David F. Donnelly. "Perinatal hyperoxia exposure impairs hypoxia-induced depolarization in rat carotid body glomus cells." Respiratory Physiology & Neurobiology 188, no. 1 (August 2013): 9–14. http://dx.doi.org/10.1016/j.resp.2013.04.016.

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33

Buckler, K. J. "A novel oxygen-sensitive potassium current in rat carotid body type I cells." Journal of Physiology 498, no. 3 (February 1, 1997): 649–62. http://dx.doi.org/10.1113/jphysiol.1997.sp021890.

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34

Bee, Denise, D. J. Palloi, and Gwenda Barer. "Division of Type I and Endothelial Cells in the Hypoxic Rat Carotid Body." Cells Tissues Organs 126, no. 4 (1986): 226–29. http://dx.doi.org/10.1159/000146222.

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35

Silva, Jeane M., and Deborah L. Lewis. "Nitric oxide enhances Ca2+-dependent K+ channel activity in rat carotid body cells." Pflügers Archiv - European Journal of Physiology 443, no. 5 (March 2002): 671–75. http://dx.doi.org/10.1007/s00424-001-0745-1.

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36

Monti-Bloch, L., V. Abudara, and P. Aguilera. "Effects of dopamine on type I chemoreceptor cells of the rat carotid body." Brain Research 617, no. 1 (July 1993): 147–50. http://dx.doi.org/10.1016/0006-8993(93)90626-x.

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37

Sherpa, A. K., K. H. Albertine, D. G. Penney, B. Thompkins, and S. Lahiri. "Chronic CO exposure stimulates erythropoiesis but not glomus cell growth." Journal of Applied Physiology 67, no. 4 (October 1, 1989): 1383–87. http://dx.doi.org/10.1152/jappl.1989.67.4.1383.

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The effect of chronic CO exposure, which stimulates erythropoietin production and erythropoiesis, was studied on carotid body cells in the rat. The hypothesis to be tested was that chronic CO inhalation would stimulate cellular hypertrophy and hyperplasia of carotid body if it caused local tissue hypoxia as in chronic hypoxia. The failure of an appropriate response would indicate a lack of a specific local effect on carotid body tissue PO2 presumably because of its unusually high tissue blood flow. Six young male rats were exposed to 0.4–0.5 Torr (0.05–0.07%) inspired PCO in air for 22 days. Control rats (n = 6) were maintained under similar conditions except for CO exposure. After the exposure period the rats were anesthetized, blood was collected for hematocrit, and the carotid bodies were surgically exposed and fixed for electron microscopy and morphometry of type I and type II cells and capillary endothelium. Hematocrit was significantly greater in the CO-exposed group (75 vs. 48%), whereas no significant difference was found in the carotid body parenchyma between the control and CO-exposed groups. We conclude that the lack of an effect of chronic CO exposure on the carotid bodies in contrast to the strong erythropoietic response indicates a relatively high tissue blood flow rate in the carotid body and that CO did not exert a direct cellular effect. The results also suggest that the hypertrophic response of carotid body glomus cells to chronic hypoxic hypoxia is the result of a local direct effect of low PO2 rather than secondary to systemic effects.

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Pawar, Anita, Ying-Jie Peng, Frank J. Jacono, and Nanduri R. Prabhakar. "Comparative analysis of neonatal and adult rat carotid body responses to chronic intermittent hypoxia." Journal of Applied Physiology 104, no. 5 (May 2008): 1287–94. http://dx.doi.org/10.1152/japplphysiol.00644.2007.

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Previous studies suggest that carotid body responses to long-term changes in environmental oxygen differ between neonates and adults. In the present study we tested the hypothesis that the effects of chronic intermittent hypoxia (CIH) on the carotid body differ between neonates and adult rats. Experiments were performed on neonatal (1–10 days) and adult (6–8 wk) males exposed either to CIH (9 episodes/h; 8 h/day) or to normoxia. Sensory activity was recorded from ex vivo carotid bodies. CIH augmented the hypoxic sensory response (HSR) in both groups. The magnitude of CIH-evoked hypoxic sensitization was significantly greater in neonates than in adults. Seventy-two episodes of CIH were sufficient to evoke hypoxic sensitization in neonates, whereas as many as 720 CIH episodes were required in adults, suggesting that neonatal carotid bodies are more sensitive to CIH than adult carotid bodies. CIH-induced hypoxic sensitization was reversed in adult rats after reexposure to 10 days of normoxia, whereas the effects of neonatal CIH persisted into adult life (2 mo). Acute intermittent hypoxia (IH) evoked sensory long-term facilitation of the carotid body activity (sensory LTF, i.e., increased baseline neural activity following acute IH) in CIH-exposed adults but not in neonates. The effects of CIH were associated with hyperplasia of glomus cells in neonatal but not in adult carotid bodies. These observations demonstrate that responses to CIH differ between neonates and adults with regard to the magnitude of sensitization of HSR, susceptibility to CIH, induction of sensory LTF, reversibility of the responses, and morphological remodeling of the chemoreceptor tissue.

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Makarenko, Vladislav V., Jayasri Nanduri, Gayatri Raghuraman, Aaron P. Fox, Moataz M. Gadalla, Ganesh K. Kumar, Solomon H. Snyder, and Nanduri R. Prabhakar. "Endogenous H2S is required for hypoxic sensing by carotid body glomus cells." American Journal of Physiology-Cell Physiology 303, no. 9 (November 1, 2012): C916—C923. http://dx.doi.org/10.1152/ajpcell.00100.2012.

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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.

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Kummer, W., and H. Acker. "Immunohistochemical demonstration of four subunits of neutrophil NAD(P)H oxidase in type I cells of carotid body." Journal of Applied Physiology 78, no. 5 (May 1, 1995): 1904–9. http://dx.doi.org/10.1152/jappl.1995.78.5.1904.

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We demonstrate, by means of immunohistochemistry, that type I cells of human, guinea pig, and rat carotid bodies react with antisera raised against the subunits p22phox, gp91phox, p47phox, and p67phox of the NAD(P)H oxidase isolated from human neutrophil granulocytes. The findings support previous photometric studies that indicate that carotid body type I cells possess a putative oxygen sensor protein that is similar to the neutrophil NAD(P)H oxidase and consists of a hydrogen peroxide generating low-potential cytochrome b558 with cofactors regulating the electron transfer to oxygen.

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41

Gauda, Estelle B., Reed Cooper, Patrice K. Akins, and Guimei Wu. "Prenatal nicotine affects catecholamine gene expression in newborn rat carotid body and petrosal ganglion." Journal of Applied Physiology 91, no. 5 (November 1, 2001): 2157–65. http://dx.doi.org/10.1152/jappl.2001.91.5.2157.

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Nicotine exposure modifies the expression of catecholamine and opioid neurotransmitter systems involved in attenuation of hypoxic chemosensitivity. We used in situ hybridization histochemistry to determine the effect of prenatal and early postnatal nicotine exposure on tyrosine hydroxylase (TH), dopamine β-hydroxylase (DβH), preproenkephalin (PPE), and D2-dopamine receptor mRNA levels in the rat carotid body and petrosal ganglion during postnatal development. In the carotid body, nicotine increased TH mRNA expression in animals at 0 and 3 postnatal days (both, P < 0.05 vs. control) without affecting TH mRNA levels at 6 and 15 days. At 15 postnatal days, DβH mRNA levels were increased in the carotid body of nicotine-exposed animals. Dopamine D2-receptor mRNA levels in the carotid body increased with postnatal age but were unaffected by nicotine exposure. PPE was not expressed in the carotid body at any of the ages studied in control or treated animals. In the petrosal ganglion, nicotine increased the number of ganglion cells expressing TH mRNA in animals at 3 days ( P < 0.01 vs. control). DβH mRNA expression was not induced nor was PPE mRNA expression increased in the petrosal ganglion in treated animals. Prenatal nicotine exposure upregulates mRNAs involved in the synthesis of two inhibitory neuromodulators, dopamine and norepinephrine, in peripheral arterial chemoreceptors, which may contribute to abnormalities in cardiorespiratory control observed in nicotine exposed animals.

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Mokashi, A., D. Ray, F. Botre, M. Katayama, S. Osanai, and S. Lahiri. "Effect of hypoxia on intracellular pH of glomus cells cultured from cat and rat carotid bodies." Journal of Applied Physiology 78, no. 5 (May 1, 1995): 1875–81. http://dx.doi.org/10.1152/jappl.1995.78.5.1875.

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To test the hypothesis that hypoxia may induce cellular acidification during chemotransduction in the carotid body, we compared the effects of hypoxia and of extracellular acidosis on intracellular pH (pHi) of glomus cells cultured from rat and cat carotid bodies. The cells were prepared and cultured for 2–7 days. The plated cells were loaded with a pH-sensitive fluorescent probe, SNARF-1-acetoxymethyl ester, and were placed in a closed chamber and superfused. The effects of lowering PO2 and pH in the superfusion medium containing CO2-HCO3- buffer on the glomus cell pHi were measured at 37 degrees C. The pHi was measured in a single or a few isolated cells with single excitation at 540 nm and dual emission at 590 and 640 nm, after the exposure to different PO2 levels from 132 to 43, 14, and 1–2 Torr for 10–12 min in the closed chamber. The resting pHi values were 7.263 +/- 0.008 for rat and 7.175 +/- 0.004 for cat carotid body glomus cells. For a decrease of PO2 from 132 Torr to 14 Torr, the change in pHi values, on average, for cat and rat glomus cells was 0.034 lower, and with PO2 decrease to 1–2 Torr for the cat glomus cells, the change in pHi values was 0.051 lower. On the other hand, when the perfusate pH values were decreased from 7.4 to 6.9 during normoxia, the reduction of change in pHi values were 0.327 for the rat and 0.397 for the cat. Thus glomus cell pHi change due to low PO2 exposure was not significant and was not commensurate with the large increases in the chemosensory activity.

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Holt, Andrew W., and David A. Tulis. "Experimental Rat and Mouse Carotid Artery Surgery: Injury and Remodeling Studies." ISRN Minimally Invasive Surgery 2013 (May 14, 2013): 1–10. http://dx.doi.org/10.1155/2013/167407.

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In cardiovascular research, translation of benchtop findings to the whole body environment is often critical in order to gain a more thorough and comprehensive clinical evaluation of the data with direct extrapolation to the human condition. In particular, developmental and/or pathophysiologic vascular growth studies often employ in vitro approaches such as cultured cells or tissue explant models in order to analyze specific cellular, molecular, genetic, and/or biochemical signaling factors under pristine controlled conditions. However, validation of in vitro data in a whole body setting complete with neural, endocrine, and other systemic contributions provides an essential proof of concept from a clinical perspective. Several well-characterized experimental in vivo models exist that provide excellent proof-of-concept tools to examine vascular growth and remodeling in the whole body. This paper will examine the rat carotid artery balloon injury model, the mouse carotid artery wire denudation injury model, and rat and mouse carotid artery ligation models with particular emphasis on minimally invasive surgical access to the site of intervention. Discussion will include key scientific and technical details as well as caveats, limitations, and considerations for the practical use of each of these valuable experimental models.

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Donnelly, D. F. "Electrochemical detection of catecholamine release from rat carotid body in vitro." Journal of Applied Physiology 74, no. 5 (May 1, 1993): 2330–37. http://dx.doi.org/10.1152/jappl.1993.74.5.2330.

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Neurotransmitter secretion from carotid body glomus cells is hypothesized to be an essential element of chemotransduction. To address one aspect of this hypothesis, catecholamine release in response to hypoxic hypoxia and histotoxic hypoxia was examined using electrically treated carbon-fiber microelectrodes placed in rat carotid bodies in vitro. Carotid bodies of mature rats were removed, along with a portion of the sinus nerve, and suspended in oxygenated (95% O2–5% CO2) Ringer saline at 35 degrees C. The microelectrode differential current after a 50-mV step was recorded over the potential range of -300 to +500 mV. In some preparations, a suction electrode applied to the sinus nerve recorded single-fiber chemoreceptor afferent activity. Stimulation by severe hypoxia (Po2 approximately 0–10 Torr for 3 min, n = 10) and cyanide (2 mM for 2 min) caused an increase in sinus nerve activity and an increase in the carbon-fiber electrode current at a potential corresponding to the oxidation potential of dopamine. As measured in the amperometric mode (constant voltage), tissue catecholamine was 0.35 +/- 0.05 microM (n = 6) and increased to 1.64 +/- 0.43 microM by 1 min of severe hypoxia or to 1.06 +/- 0.17 microM at 2 min of moderate hypoxia (Po2 approximately 50 Torr). Exposure to calcium-free Ringer saline before hypoxia ablated the increase in electrode current, and the response was restored after reperfusion with calcium-containing saline. Repeated exposures to hypoxia (3-min duration) every 15 min resulted in significantly smaller nerve and catecholamine responses. By the third hypoxia exposure, nerve and catecholamine responses were diminished by 30–50%.

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Liu, X., L. He, L. Stensaas, B. Dinger, and S. Fidone. "Adaptation to chronic hypoxia involves immune cell invasion and increased expression of inflammatory cytokines in rat carotid body." American Journal of Physiology-Lung Cellular and Molecular Physiology 296, no. 2 (February 2009): L158—L166. http://dx.doi.org/10.1152/ajplung.90383.2008.

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Exposure to chronic hypoxia (CH; 3–28 days at 380 Torr) induces adaptation in mammalian carotid body such that following CH an acute hypoxic challenge elicits an abnormally large increase in carotid sinus nerve impulse activity. The current study examines the hypothesis that CH initiates an immune response in the carotid body and that chemoreceptor hyperexcitability is dependent on the expression and action of inflammatory cytokines. CH resulted in a robust invasion of ED1+ macrophages, which peaked on day 3 of exposure. Gene expression of proinflammatory cytokines, IL-1β, TNFα, and the chemokine, monocyte chemoattractant protein-1, was increased >2-fold after 1 day of hypoxia followed by a >2-fold increase in IL-6 on day 3. After 28 days of CH, IL-6 remained elevated >5-fold, whereas expression of other cytokines recovered to normal levels. Cytokine expression was not restricted to immune cells. Studies of cultured type I cells harvested following 1 day of in vivo hypoxia showed elevated transcript levels of inflammatory cytokines. In situ hybridization studies confirmed expression of IL-6 in type I cells and also showed that CH induces IL-6 expression in supporting type II cells. Concurrent treatment of CH rats with anti-inflammatory drugs (ibuprofen or dexamethasone) blocked immune cell invasion and severely reduced CH-induced cytokine expression in carotid body. Drug treatment also blocked the development of chemoreceptor hypersensitivity in CH animals. Our findings indicate that chemoreceptor adaptation involves novel neuroimmune mechanisms, which may alter the functional phenotypes of type I cells and chemoafferent neurons.

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Thompson, Carrie M., Keith Troche, Heidi L. Jordan, Barbara L. Barr, and Christopher N. Wyatt. "Evidence for functional, inhibitory, histamine H3 receptors in rat carotid body Type I cells." Neuroscience Letters 471, no. 1 (February 2010): 15–19. http://dx.doi.org/10.1016/j.neulet.2009.12.077.

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Carpenter, E., and C. Peers. "Swelling- and cAMP-Activated Cl−Currents in Isolated Rat Carotid Body Type I Cells." Journal of Physiology 503, no. 3 (September 1997): 497–511. http://dx.doi.org/10.1111/j.1469-7793.1997.497bg.x.

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Ortiz, Fernando C., and Rodrigo Varas. "Muscarinic modulation of TASK-like background potassium channel in rat carotid body chemoreceptor cells." Brain Research 1323 (April 2010): 74–83. http://dx.doi.org/10.1016/j.brainres.2010.01.091.

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Buttigieg, Josef, and Colin A. Nurse. "Detection of hypoxia-evoked ATP release from chemoreceptor cells of the rat carotid body." Biochemical and Biophysical Research Communications 322, no. 1 (September 2004): 82–87. http://dx.doi.org/10.1016/j.bbrc.2004.07.081.

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Donnelly, David F. "Response to cyanide of two types of glomoid cells in mature rat carotid body." Brain Research 630, no. 1-2 (December 1993): 157–68. http://dx.doi.org/10.1016/0006-8993(93)90653-5.

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Journal articles on the topic 'Rat carotid body cells'

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