scholarly journals Sensory Processing and Integration at the Carotid Body Tripartite Synapse: Neurotransmitter Functions and Effects of Chronic Hypoxia

2018 ◽  
Vol 9 ◽  
Author(s):  
Erin M. Leonard ◽  
Shaima Salman ◽  
Colin A. Nurse
Keyword(s):  
Sensory Processing ◽  
Carotid Body ◽  
Chronic Hypoxia ◽  
Tripartite Synapse

scholarly journals An O2-Sensitive Glomus Cell-Stem Cell Synapse Induces Carotid Body Growth in Chronic Hypoxia

Cell ◽  
2014 ◽  
Vol 156 (1-2) ◽  
pp. 291-303 ◽  
Author(s):  
Aida Platero-Luengo ◽  
Susana González-Granero ◽  
Rocío Durán ◽  
Blanca Díaz-Castro ◽  
José I. Piruat ◽  
...  
Keyword(s):  
Stem Cell ◽  
Carotid Body ◽  
Chronic Hypoxia ◽  
Body Growth ◽  
Glomus Cell ◽  
Cell Synapse ◽  
Cell Stem Cell

Does chronic hypoxia increase rat carotid body nitric oxide?

1998 ◽  
Vol 120 (2) ◽  
pp. 243-247 ◽  
Author(s):  
C. Di Giulio ◽  
A. Grilli ◽  
M.A. De Lutiis ◽  
F. Di Natale ◽  
G. Sabatino ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Carotid Body ◽  
Chronic Hypoxia

scholarly journals Modulation of chronic hypoxia-induced chemoreceptor hypersensitivity by NADPH oxidase subunits in rat carotid body

2010 ◽  
Vol 108 (5) ◽  
pp. 1304-1310 ◽  
Author(s):  
L. He ◽  
X. Liu ◽  
J. Chen ◽  
B. Dinger ◽  
L. Stensaas ◽  
...  
Keyword(s):  
Nadph Oxidase ◽  
Carotid Body ◽  
Chronic Hypoxia ◽  
Body Tissue ◽  
Regulatory Subunit ◽  
Type I ◽  
Ros Production ◽  
Tissue Slices ◽  
Type I Cells ◽  
I Cells

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.

Breathing periodicity in intact and carotid body-denervated ponies during normoxia and chronic hypoxia

1993 ◽  
Vol 74 (3) ◽  
pp. 1073-1082 ◽  
Author(s):  
D. R. Brown ◽  
H. V. Forster ◽  
A. S. Greene ◽  
T. F. Lowry
Keyword(s):  
Carotid Body ◽  
Chronic Hypoxia ◽  
Pulmonary Ventilation ◽  
Periodic Breathing ◽  
Total Power ◽  
Fast Fourier Transformation ◽  
Periodic Oscillations ◽  
Carotid Chemoreceptors ◽  
Induced Changes ◽  
Arterial Po2

Periodic oscillations in pulmonary ventilation (VI), tidal volume (VT), and inspiratory and expiratory times (TI and TE) were studied during normoxia (arterial PO2 = 95 Torr) and 48 h of hypoxia (arterial PO2 = 40–50 Torr) in awake intact (n = 8) and carotid body-denervated (CBD; n = 8) ponies. Periodic oscillations were identified by fast-Fourier transformation of breath-by-breath data and quantitated by determining the power ratio of significant periodic oscillations to total power of data sequence. Periodic oscillations of 0.063–0.500 cycles/breath were observed in all parameters during both normoxia and hypoxia. During normoxia, CBD accentuated periodicity of VT (P < 0.02) and VI (P < 0.01) but did not change TI or TE periodicity (P > 0.05). These findings suggest that carotid chemoreceptors serve to stabilize breathing (i.e., decrease periodicity) during normoxia, conceivably because of their shorter response time compared with that of central chemoreceptors. During certain periods of hypoxia, periodicity of VT and VI was significantly (P < 0.05) increased in intact ponies. The response to hypoxia in CBD ponies was variable, with VI periodicity significantly (P < 0.05) increasing, decreasing, or unchanging. Because some CBD ponies significantly changed their periodicity during hypoxia compared with normoxia, we conclude that carotid chemoreceptors are not requisite for hypoxia-induced changes in periodic breathing. In addition, our observations in both groups of ponies during normoxia and hypoxia suggest that multiple mechanisms may lead to periodic oscillations in breathing.

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