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Journal articles on the topic 'Rat carotid body cells'

Author: Grafiati

Published: 4 June 2021

Last updated: 13 February 2022

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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 (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 recepto

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2

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 (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/

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3

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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4

Martinez, A., L. Saldise, MJ Ramirez, et al. "Adrenomedullin expression and function in the rat carotid body." Journal of Endocrinology 176, no. 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

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5

Makarenko, Vladislav V., Ying-Jie Peng, Guoxiang Yuan, et al. "CaV3.2 T-type Ca2+ channels in H2S-mediated hypoxic response of the carotid body." American Journal of Physiology-Cell Physiology 308, no. 2 (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 bl

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6

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 (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

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7

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 (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 (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

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9

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 (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

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10

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 (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-substitutio

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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 (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 flu

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12

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

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13

Wang, Xi, Bai-Ren Wang, Xiao-Li Duan, et al. "Strong Expression of Interleukin-1 Receptor Type I in the Rat Carotid Body." Journal of Histochemistry & Cytochemistry 50, no. 12 (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,

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14

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 (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

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15

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 (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 ne

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16

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 (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 ce

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17

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 (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

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18

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 (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 hydroxyla

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19

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 (1994): 559–64. http://dx.doi.org/10.1007/s004410050118.

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20

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 (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 fou

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21

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 (2004): 493–500. http://dx.doi.org/10.1111/j.1471-4159.2004.02740.x.

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22

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 (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) m

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23

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 (2003): 789–800. http://dx.doi.org/10.1113/jphysiol.2003.039693.

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24

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 (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

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25

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 (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

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26

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 (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

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27

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 (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 show

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28

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 (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(

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29

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 (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 (

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30

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 (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 (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 (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 (1997): 649–62. http://dx.doi.org/10.1113/jphysiol.1997.sp021890.

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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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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 (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 (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 (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. C

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38

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 (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 sensiti

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39

Makarenko, Vladislav V., Jayasri Nanduri, Gayatri Raghuraman, et al. "Endogenous H2S is required for hypoxic sensing by carotid body glomus cells." American Journal of Physiology-Cell Physiology 303, no. 9 (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

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40

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 (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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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 (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

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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 (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 deg

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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 compl

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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 (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

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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 (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 chemok

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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 (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 (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 (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 (1993): 157–68. http://dx.doi.org/10.1016/0006-8993(93)90653-5.

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