The Human Carotid Body

Fagerlund, Malin Jonsson; Kåhlin, Jessica; Ebberyd, Anette; Schulte, Gunnar; Mkrtchian, Souren; Eriksson, Lars

doi:10.1097/aln.0b013e3181fac061

Cited by 52 publications

(22 citation statements)

References 42 publications

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“…This K B channel is highly expressed in the type I cell where its properties support the existence of TASK-1-like (112) and TASK-3-like (911) subunit activities that are likely a consequence of a TASK1/3 heterodimer that contributes the principal component of the K B conductance (438, 441). In addition, TASK-2 and TWIK-related arachidonic acid-stimulated K + channel (TRAAK) have also been localized by immunohistochemisty to the type I cell (928) and TASK-1 immunoreactivity has also been reported in the mouse carotid body (423) and human carotid body (261) as well as on rat type II cells (485), although their function on these latter cells has not been determined. The channel has a characteristic, low conductance of ca .…”

Section: Sensing Hypoxia—transduction Processes In the Carotid Bodymentioning

confidence: 99%

Peripheral Chemoreceptors: Function and Plasticity of the Carotid Body

Kumar

Prabhakar

2012

Comprehensive Physiology

453

572

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The discovery of the sensory nature of the carotid body dates back to the beginning of the 20th century. Following these seminal discoveries, research into carotid body mechanisms moved forward progressively through the 20th century, with many descriptions of the ultrastructure of the organ and stimulus-response measurements at the level of the whole organ. The later part of 20th century witnessed the first descriptions of the cellular responses and electrophysiology of isolated and cultured type I and type II cells, and there now exist a number of testable hypotheses of chemotransduction. The goal of this article is to provide a comprehensive review of current concepts on sensory transduction and transmission of the hypoxic stimulus at the carotid body with an emphasis on integrating cellular mechanisms with the whole organ responses and highlighting the gaps or discrepancies in our knowledge. It is increasingly evident that in addition to hypoxia, the carotid body responds to a wide variety of blood-borne stimuli, including reduced glucose and immune-related cytokines and we therefore also consider the evidence for a polymodal function of the carotid body and its implications. It is clear that the sensory function of the carotid body exhibits considerable plasticity in response to the chronic perturbations in environmental O2 that is associated with many physiological and pathological conditions. The mechanisms and consequences of carotid body plasticity in health and disease are discussed in the final sections of this article.

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Section: Sensing Hypoxia—transduction Processes In the Carotid Bodymentioning

confidence: 99%

Peripheral Chemoreceptors: Function and Plasticity of the Carotid Body

Kumar

Prabhakar

2012

Comprehensive Physiology

453

572

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“…Recent studies show that TASK-1, but not TASK-3, is expressed in the human carotid body, as judged by mRNA and protein expression (Fagerlund et al , 2010) and microarray studies (Mkrtcian et al, 2012), suggesting that TASK-1, not TASK-1/3 heteromer, may be the background K 2P channel in human glomus cells. The significance of expression of TASK-1 vs. TASK-3 or TASK-1/3 is not obvious, as they all behave as background K + channels.…”

Section: Task-1 and Task-3 Channels (K2p31 And K2p91)mentioning

confidence: 99%

K+ channels in O2 sensing and postnatal development of carotid body glomus cell response to hypoxia

Kim¹

2013

Respiratory Physiology & Neurobiology

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The sensitivity of carotid body chemoreceptors to hypoxia is low just after birth and increases over the first few weeks of the postnatal period. At present, it is believed that the hypoxia-induced excitation of carotid body glomus cells begins with the inhibition of the outward K+ current via one or more O2 sensors. Although the nature of the O2 sensors and their signals that inhibit the K+ current are not well defined, studies suggest that the postnatal maturation of the glomus cell response to hypoxia is largely due to the increased sensitivity of K+ channels to hypoxia. As KV, BK and TASK channels that are O2-sensitive contribute to the K+ current, it is important to identify the O2 sensor and the signaling molecule for each of these K+ channels. Various O2 sensors (mitochondrial hemeprotein, hemeoxygenase-2, NADPH oxidase) and associated signals have been proposed to mediate the inhibition of K+ channels by hypoxia. Studies suggest that a mitochondrial hemeprotein is likely to serve as an O2 sensor for K+ channels, particularly for TASK, and that multiple signals may be involved. Thus, changes in the sensitivity of the mitochondrial O2 sensor to hypoxia, the sensitivity of K+ channels to signals generated by mitochondria, and/or the expression levels of K+ channels are likely to account for the postnatal maturation of O2 sensing by glomus cells.

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“…Dopaminergic D 2 receptors are located in the carotid bodies in hamsters within the glomus cells (Schlenker, unpublished observations) and within several brain regions associated with control of breathing including nucleus tractus solitaires (NTS), the paraventicular nucleus of the hypothalamus (PVN) and in the striatum (Fagerlund et al, 2010; Kline et al, 2002; Weiner et al, 1991). Both the NTS and the PVN are integratory regions that help regulate ventilatory responses to hypoxia (Genest et al, 2007; Granjeiro and Machado, 2009; Reddy et al, 2005; Schlenker et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

Hypothyroidism stimulates D2 receptor-mediated breathing in response to acute hypoxia and alters D2 receptors levels in carotid bodies and brain

Schlenker

Schultz

2012

Respiratory Physiology & Neurobiology

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Hypothyroidism can depress breathing and alter dopamine D2 receptor expression and function. We hypothesized that relative to euthyroid hamsters (EH), hypothyroid hamsters (HH) contain increased D2 receptors in brain regions associated with breathing and carotid bodies (CB), and that stimulation of D2 receptors would decease ventilation more in the HH compared to the EH. Hamsters were treated with vehicle, carmoxirile (peripherally acting D2 receptor agonist), or bromocriptine (central and peripherally acting D2 receptor agonist) and breathing was evaluated during exposure to air, hypoxia, and then air. HH exhibited increased D2 receptor protein levels in the striatum and CB’s, but decreased levels in the paraventricular hypothalamic nucleus. Relative to vehicle, carmoxirole and bromocriptine stimulated ventilation in the HH during and following exposure to hypoxia. Only bromocriptine depressed ventilation in the EH during and after exposure to hypoxia. Thus,, hypothyroidism impacts the expression of D2 receptors in the carotid body, PVN and striatum, and D2 stimulation affects ventilation remarkably differently than in EH.

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The Human Carotid Body

Cited by 52 publications

References 42 publications

Peripheral Chemoreceptors: Function and Plasticity of the Carotid Body

Peripheral Chemoreceptors: Function and Plasticity of the Carotid Body

K+ channels in O2 sensing and postnatal development of carotid body glomus cell response to hypoxia

Hypothyroidism stimulates D2 receptor-mediated breathing in response to acute hypoxia and alters D2 receptors levels in carotid bodies and brain

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