scholarly journals Carotid body overactivity induces respiratory neurone channelopathy contributing to neurogenic hypertension

2015 ◽  
Vol 593 (14) ◽  
pp. 3055-3063 ◽  
Author(s):  
Davi J. A. Moraes ◽  
Benedito H. Machado ◽  
Julian F. R. Paton
Keyword(s):  
Carotid Body ◽  
Neurogenic Hypertension ◽  
Respiratory Neurone

scholarly journals The carotid body as a putative therapeutic target for the treatment of neurogenic hypertension

2013 ◽  
Vol 4 (1) ◽  
Author(s):  
Fiona D. McBryde ◽  
Ana P. Abdala ◽  
Emma B. Hendy ◽  
Wioletta Pijacka ◽  
Paul Marvar ◽  
...  
Keyword(s):  
Carotid Body ◽  
Therapeutic Target ◽  
Neurogenic Hypertension

scholarly journals Purinergic plasticity within petrosal neurons in hypertension

2018 ◽  
Vol 315 (5) ◽  
pp. R963-R971 ◽  
Author(s):  
Davi J. A. Moraes ◽  
Melina P. da Silva ◽  
Pedro F. Spiller ◽  
Benedito H. Machado ◽  
Julian F. R. Paton
Keyword(s):  
Carotid Body ◽  
Atp Release ◽  
Clinical Importance ◽  
Receptor Expression ◽  
P2x3 Receptors ◽  
Neurogenic Hypertension ◽  
Factors Affecting ◽  
Electrophysiological Properties ◽  
Carotid Bodies ◽  
Clinical Interest

The carotid bodies are peripheral chemoreceptors and contribute to the homeostatic maintenance of arterial levels of O2, CO2, and [H+]. They have attracted much clinical interest recently because of the realization that aberrant signaling in these organs is associated with several pathologies including hypertension. Herein, we describe data suggesting that sympathetic overactivity in neurogenic hypertension is, at least in part, dependent on carotid body tonicity and hyperreflexia that is related to changes in the electrophysiological properties of chemoreceptive petrosal neurons. We present results showing critical roles for both ATP levels in the carotid bodies and expression of P2X3 receptors in petrosal chemoreceptive, but not baroreceptive, terminals in the etiology of carotid body tonicity and hyperreflexia. We discuss mechanisms that may underlie the changes in electrophysiological properties and P2X3 receptor expression in chemoreceptive petrosal neurons, as well as factors affecting ATP release by cells within the carotid bodies. Our findings support the notion of targeting the carotid bodies to reduce sympathetic outflow and arterial pressure, emphasizing the potential clinical importance of modulating purinergic transmission to treat pathologies associated with carotid body dysfunction but, importantly, sparing physiological chemoreflex function.

scholarly journals G-Protein-Coupled Receptor (GPCR) Signaling in the Carotid Body: Roles in Hypoxia and Cardiovascular and Respiratory Disease

2020 ◽  
Vol 21 (17) ◽  
pp. 6012 ◽  
Author(s):  
Hayyaf S. Aldossary ◽  
Abdulaziz A. Alzahrani ◽  
Demitris Nathanael ◽  
Eyas A. Alhuthail ◽  
Clare J. Ray ◽  
...  
Keyword(s):  
G Protein ◽  
Respiratory Disease ◽  
Carotid Body ◽  
Carotid Bifurcation ◽  
Neurogenic Hypertension ◽  
Downstream Effects ◽  
Obstructive Sleep ◽  
G Protein Coupled ◽  
The Brain ◽  
Major Target

The carotid body (CB) is an important organ located at the carotid bifurcation that constantly monitors the blood supplying the brain. During hypoxia, the CB immediately triggers an alarm in the form of nerve impulses sent to the brain. This activates protective reflexes including hyperventilation, tachycardia and vasoconstriction, to ensure blood and oxygen delivery to the brain and vital organs. However, in certain conditions, including obstructive sleep apnea, heart failure and essential/spontaneous hypertension, the CB becomes hyperactive, promoting neurogenic hypertension and arrhythmia. G-protein-coupled receptors (GPCRs) are very highly expressed in the CB and have key roles in mediating baseline CB activity and hypoxic sensitivity. Here, we provide a brief overview of the numerous GPCRs that are expressed in the CB, their mechanism of action and downstream effects. Furthermore, we will address how these GPCRs and signaling pathways may contribute to CB hyperactivity and cardiovascular and respiratory disease. GPCRs are a major target for drug discovery development. This information highlights specific GPCRs that could be targeted by novel or existing drugs to enable more personalized treatment of CB-mediated cardiovascular and respiratory disease.

Fine Structure of Carotid Body: Normal and Anoxic Cats

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

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

Onyx Embolization of Carotid Body Paragangliomas: An Adjunct to Safe and Effective Surgical Resection

2013 ◽  
Vol 74 (S 01) ◽  
Author(s):  
Felipe Albuquerque ◽  
Cameron McDougall ◽  
Robert Spetzler ◽  
Andrew Ducruet ◽  
Webster Crowley ◽  
...  
Keyword(s):  
Surgical Resection ◽  
Carotid Body
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