Voltage- and receptor-mediated activation of a non-selective cation channel in rat carotid body glomus cells

Wang, Jiaju; Hogan, James O.; Kim, Dong‐Hee

doi:10.1016/j.resp.2016.12.005

Cited by 8 publications

(9 citation statements)

References 49 publications

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“…Recent evidence has revealed the presence of TRP and other non-selective Ca 2+ -activated cation currents in type I cells that are activated by hypoxia ( Kumar et al, 2006 ; Kang et al, 2014 ; Kim I. et al, 2015 ; Wang et al, 2017a ). Although intriguing, the full functional relevance of these currents in type I cell O 2 -sensing remains to be further characterized, and in particular whether these currents can be upregulated to preserve O 2 sensing in the absence of TASK channels ( Turner and Buckler, 2013 ).…”

Section: Mitochondrial Inhibitors Mimic All Aspects Of the Carotid Bomentioning

confidence: 99%

“…Although intriguing, the full functional relevance of these currents in type I cell O 2 -sensing remains to be further characterized, and in particular whether these currents can be upregulated to preserve O 2 sensing in the absence of TASK channels ( Turner and Buckler, 2013 ). Current evidence suggests that mitochondrial inhibitors are also capable of increasing these inward depolarizing currents ( Kim I. et al, 2015 ; Wang et al, 2017a ).…”

Section: Mitochondrial Inhibitors Mimic All Aspects Of the Carotid Bomentioning

confidence: 99%

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Is Carotid Body Physiological O2 Sensitivity Determined by a Unique Mitochondrial Phenotype?

et al. 2018

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The mammalian carotid body (CB) is the primary arterial chemoreceptor that responds to acute hypoxia, initiating systemic protective reflex responses that act to maintain O2 delivery to the brain and vital organs. The CB is unique in that it is stimulated at O2 levels above those that begin to impact on the metabolism of most other cell types. Whilst a large proportion of the CB chemotransduction cascade is well defined, the identity of the O2 sensor remains highly controversial. This short review evaluates whether the mitochondria can adequately function as acute O2 sensors in the CB. We consider the similarities between mitochondrial poisons and hypoxic stimuli in their ability to activate the CB chemotransduction cascade and initiate rapid cardiorespiratory reflexes. We evaluate whether the mitochondria are required for the CB to respond to hypoxia. We also discuss if the CB mitochondria are different to those located in other non-O2 sensitive cells, and what might cause them to have an unusually low O2 binding affinity. In particular we look at the potential roles of competitive inhibitors of mitochondrial complex IV such as nitric oxide in establishing mitochondrial and CB O2-sensitivity. Finally, we discuss novel signaling mechanisms proposed to take place within and downstream of mitochondria that link mitochondrial metabolism with cellular depolarization.

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Section: Mitochondrial Inhibitors Mimic All Aspects Of the Carotid Bomentioning

confidence: 99%

Section: Mitochondrial Inhibitors Mimic All Aspects Of the Carotid Bomentioning

confidence: 99%

Is Carotid Body Physiological O2 Sensitivity Determined by a Unique Mitochondrial Phenotype?

et al. 2018

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“…The paracrine effects of ET-1 on glomus cells [ 110 ] and type II cells [ 111 ] were investigated by ratiometric Ca 2+ imaging. Intriguingly, different results were reported for type I and type II cells, although in different studies.…”

Section: Endothelinsmentioning

confidence: 99%

“…Intriguingly, different results were reported for type I and type II cells, although in different studies. ET-1 produced either no or very weak increase in [Ca 2+ ] into CB glomus cells at a concentration of 10 nM [ 110 ]. Conversely, lower concentrations of ET-1 (1 nM) induced robust intracellular Ca 2+ responses in subpopulations of type II cells [ 111 ].…”

Section: Endothelinsmentioning

confidence: 99%

Growth Factors in the Carotid Body—An Update

Stocco

Barbon

Tortorella

et al. 2020

IJMS

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The carotid body may undergo plasticity changes during development/ageing and in response to environmental (hypoxia and hyperoxia), metabolic, and inflammatory stimuli. The different cell types of the carotid body express a wide series of growth factors and corresponding receptors, which play a role in the modulation of carotid body function and plasticity. In particular, type I cells express nerve growth factor, brain-derived neurotrophic factor, neurotrophin 3, glial cell line-derived neurotrophic factor, ciliary neurotrophic factor, insulin-like-growth factor-I and -II, basic fibroblast growth factor, epidermal growth factor, transforming growth factor-α and -β, interleukin-1β and -6, tumor necrosis factor-α, vascular endothelial growth factor, and endothelin-1. Many specific growth factor receptors have been identified in type I cells, indicating autocrine/paracrine effects. Type II cells may also produce growth factors and express corresponding receptors. Future research will have to consider growth factors in further experimental models of cardiovascular, metabolic, and inflammatory diseases and in human (normal and pathologic) samples. From a methodological point of view, microarray and/or proteomic approaches would permit contemporary analyses of large groups of growth factors. The eventual identification of physical interactions between receptors of different growth factors and/or neuromodulators could also add insights regarding functional interactions between different trophic mechanisms.

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“…AT 1 -receptors are coupled to the G αq protein and its activation leads to the generation of IP 3 , via phospholipase C, causing the release of Ca 2+ from intracellular stores [ 92 ]. It is now thought that this rise in Ca 2+ is sufficient to activate the non-selective cation channel which contributes to cellular depolarization [ 93 ]. Repetitive application of Ang II can also promote sensory long-term facilitation (sLTF) of chemoafferent nerve activity, an effect reliant on activation of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase and ROS generation [ 89 ].…”

Section: G αQ -Protein-coupled Receptor Signalimentioning

confidence: 99%

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

Aldossary

Alzahrani

Nathanael

et al. 2020

IJMS

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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.

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Voltage- and receptor-mediated activation of a non-selective cation channel in rat carotid body glomus cells

Cited by 8 publications

References 49 publications

Is Carotid Body Physiological O2 Sensitivity Determined by a Unique Mitochondrial Phenotype?

Is Carotid Body Physiological O2 Sensitivity Determined by a Unique Mitochondrial Phenotype?

Growth Factors in the Carotid Body—An Update

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

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