Purinergic plasticity within petrosal neurons in hypertension

The carotid bodies are peripheral chemoreceptors and contribute to the homeostatic maintenance of arterial levels of O , CO , and [H ]. They have attracted much clinical interest recently because of the realization that aberrant signaling in these organs is associated with several pathologies includ...

Full description

Saved in:
Bibliographic Details
Published in:American journal of physiology. Regulatory, integrative and comparative physiology integrative and comparative physiology, 2018-11, Vol.315 (5), p.R963-R971
Main Authors: Moraes, Davi J A, da Silva, Melina P, Spiller, Pedro F, Machado, Benedito H, Paton, Julian F R
Format: Article
Language:English
Subjects:
Adenosine Triphosphate - metabolism
Animals
ATP
Blood pressure
Carbon dioxide
Carotid body
Carotid Body - physiology
Cell Plasticity
Chemoreception (internal)
Chemoreceptor Cells - cytology
Chemoreceptors
Chemoreceptors (internal)
Etiology
Gene expression
Humans
Hypertension
Hypertension - physiopathology
Hypoxia - physiopathology
Neurons
Neurons - metabolism
Organs
Receptors
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:The carotid bodies are peripheral chemoreceptors and contribute to the homeostatic maintenance of arterial levels of O , CO , 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.
ISSN:0363-6119
1522-1490
DOI:10.1152/ajpregu.00142.2018