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Oxygen Delivery and Acute Hypoxia: Physiological and Clinical Considerations
Published in Anthony N. Nicholson, The Neurosciences and the Practice of Aviation Medicine, 2017
Peripheral chemoreceptors are located in the carotid bodies at the bifurcation of the common carotid artery. The carotid body contains neuron-like glomus or type 2 cells that are believed to act as the chemoreceptor, surrounded by glial-like type 1 cells. Each carotid body is normally just a few grams in weight, and the afferents join the carotid sinus nerve, which also carries afferents from the arterial baroreceptors in the nearby carotid sinus. The carotid sinus nerve is a branch of the glossopharyngeal nerve via which the afferent information from both chemoreceptors and baroreceptors passes to the nucleus of the tractus solitarius (NTS) in the brainstem. Similar chemoreceptors are found in the aortic bodies scattered around the aortic arch. Afferents from the aortic bodies pass to the NTS via the vagus nerve. Carotid bodies are stimulated by increased arterial PCO2, increased arterial hydrogen ion (reduced pH) and reduced arterial PO2. As discussed above, in humans the reflex ventilatory response to arterial hypoxia and also to acute metabolic acidosis is largely, if not solely, due to the stimulation of the carotid body chemoreceptors.
Intra-carotid body inter-cellular communication
Published in Journal of the Royal Society of New Zealand, 2023
Liam P. Argent, Aabharika Bose, Julian F. R. Paton
The list of other excitatory metabotropic receptors with functional roles in the carotid body includes the serotonin-activated 5-HT2a receptor, expressed by glomus cells. Serotonin binding to this receptor leads to protein kinase C-mediated inhibition of resting K+ conductances, as well as calcium dependent K+ conductances (Zhang et al. 2003), thus enhancing hypoxia-evoked depolarisation. 5-HT3 receptors are known to have an excitatory role in rat aortic bodies (Brophy et al. 1999), although whether they have a similar function in the carotid body remains to be seen. M1 and M2 muscarinic acetyl choline receptors (mAChRs) are known to be expressed by type I cells (Shirahata et al. 2004; Bairam et al. 2006), but, similar to 5-HT2a receptor activation, muscarinic stimulation appears to elevate type I cell [Ca2+]i (Dasso et al. 1997) via the inhibition of background K+ leak TASK channels (Ortiz and Varas 2010), suggesting that Gq-coupled mAChRs are functionally dominant in type I cells. α1 adrenoreceptors are expressed by type I cells, as well as cells of the carotid body vasculature and act to amplify the carotid sinus nerve output signal in response to hypoxia (Felippe et al. 2022). Transcripts encoding the excitatory D1 receptor have also been detected in the carotid body by quantitative-reverse transcriptase PCR (Bairam et al. 1998).
Device profile of the MobiusHD EVBA system for the treatment of resistant hypertension: overview of its mechanism of action, safety and efficacy
Published in Expert Review of Medical Devices, 2020
Mark C. Bates, Gregg W. Stone, Chao-Yin Chen, Wilko Spiering
Carotid baroreceptor physiology was first described in landmark animal studies by Hering in the 1920s and led to the discovery and mapping of the afferent nerve to a branch of the glossopharyngeal nerve (Hering’s nerve, also termed the carotid sinus nerve [CSN]) [19]. In the simplified primary arc of the central baroreflex network in regulating sympathetic activities, an increase in systemic blood pressure (BP) results in increasing afferent signaling from carotid sinus (CS) baroreceptors and subsequent inhibition of sympathetic outflow to lower BP via inhibiting neurons in the rostral ventral lateral medulla [20]. Please note that an exhaustive overview baroreceptor physiology is beyond the scope of this review but can be found in the excellent expert summary authored by Manci G and Mark AL. in 1983 [21].