Release of substance P by low oxygen in the rabbit carotid body: evidence for the involvement of calcium channels

Kim, Dong-kyu; Oh, Eui K; Summers, Beth A.; Prabhakar, Nanduri R.; Kumar, Ganesh K.

doi:10.1016/s0006-8993(00)03272-8

Cited by 30 publications

(19 citation statements)

References 48 publications

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“…For example, SP immunoreactivity is found in both glomus cells and the nerve fibers innervating the carotid body of the cat by Wang et al (1992) but only in nerve fibers of this species in studies performed by Chen et al (1986). While all published reports in the rabbit have localized SP immunoreactivity to nerve fibers within the carotid body (Wharton et al, 1980;Kim et al, 2001;Kusakabe et al, 1994), there is inconsistent data concerning whether SP immunoreactivity is localized to glomus cells of this species (Kusakabe et al, 1994). More consistent findings have been reported in the rat.…”

Section: Tachykinin Neurotransmitter Systemmentioning

confidence: 84%

“…SP immunoreactive nerve fibers appose glomus cells in the carotid body of the rat (Jacobowitz and Helke, 1997) and rabbit (Kusakabe et al, 1994). SP is released from excised rabbit carotid bodies in response to hypoxia (Kim et al, 2001). Therefore, it is possible that during hypoxia SP is released from fibers within the carotid body, then binds to the subunits of the nAChRs which results in reduced release of the inhibitory neurotransmitter, dopamine, from the glomus cell.…”

Section: Tachykinin Neurotransmitter Systemmentioning

confidence: 99%

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Gene expression in peripheral arterial chemoreceptors

Gauda

2002

Microscopy Res & Technique

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The peripheral arterial chemoreceptors of the carotid body participate in the ventilatory responses to hypoxia and hypercapnia, the arousal responses to asphyxial apnea, and the acclimatization to high altitude. In response to an excitatory stimuli, glomus cells in the carotid body depolarize, their intracellular calcium levels rise, and neurotransmitters are released from them. Neurotransmitters then bind to autoreceptors on glomus cells and postsynaptic receptors on chemoafferents of the carotid sinus nerve. Binding to inhibitory or excitatory receptors on chemoafferents control the electrical activity of the carotid sinus nerve, which provides the input to respiratory-related brainstem nuclei. We and others have used gene expression in the carotid body as a tool to determine what neurotransmitters mediate the response of peripheral arterial chemoreceptors to excitatory stimuli, specifically hypoxia. Data from physiological studies support the involvement of numerous putative neurotransmitters in hypoxic chemosensitivity. This article reviews how in situ hybridization histochemistry and other cellular localization techniques confirm, refute, or expand what is known about the role of dopamine, norepinephrine, substance P, acetylcholine, adenosine, and ATP in chemotransmission. In spite of some species differences, review of the available data support that 1). dopamine and norepinephrine are synthesized and released from glomus cells in all species and play an inhibitory role in hypoxic chemosensitivity; 2). substance P and acetylcholine are not synthesized in glomus cells of most species but may be made and released from nerve fibers innervating the carotid body in essentially all species; 3). adenosine and ATP are ubiquitous molecules that most likely play an excitatory role in hypoxic chemosensitivity.

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Section: Tachykinin Neurotransmitter Systemmentioning

confidence: 84%

Section: Tachykinin Neurotransmitter Systemmentioning

confidence: 99%

Gene expression in peripheral arterial chemoreceptors

Gauda

2002

Microscopy Res & Technique

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“…These include an assortment of vesicular-bound, biogenic amines [(ACh), DA, norepinephrine (NE), 5-HT (884, 945)], purines (ATP, adenosine), neuropeptides [enkephalins (884), substance P (439), NPY (462, 713)], calcitonin-gene related peptide (484), cholecystokinin (876), ANP (881), endothelins (354), and amino acids (GABA) (650), and enzymes generating gas transmitters including NO, CO, and H 2 S (see sections below for details regarding these three gases). Finally, both histamine (453) and angiotensin II (521) have also been localized to the carotid body where they may be involved in modulating the response to ACh (827) or the pathological changes in chemosensitivity observed in heart failure [(529); see later section], respectively.…”

Section: Neurotransmission In the Carotid Bodymentioning

confidence: 99%

Peripheral Chemoreceptors: Function and Plasticity of the Carotid Body

Kumar

Prabhakar

2012

Comprehensive Physiology

465

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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“…Early studies reported that hypoxia of the rat carotid body increased SP release as a function of the severity of the hypoxic insult [95]. This finding suggested that SP release may be a tissue response to hypoxia/ischaemia.…”

Section: Neurogenic Inflammationmentioning

confidence: 95%

The Role of Substance P in Ischaemic Brain Injury

Turner¹,

Vink²

2013

Brain Sciences

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Stroke is a leading cause of death, disability and dementia worldwide. Despite extensive pre-clinical investigation, few therapeutic treatment options are available to patients, meaning that death, severe disability and the requirement for long-term rehabilitation are common outcomes. Cell loss and tissue injury following stroke occurs through a number of diverse secondary injury pathways, whose delayed nature provides an opportunity for pharmacological intervention. Amongst these secondary injury factors, increased blood-brain barrier permeability and cerebral oedema are well-documented complications of cerebral ischaemia, whose severity has been shown to be associated with final outcome. Whilst the mechanisms of increased blood-brain barrier permeability and cerebral oedema are largely unknown, recent evidence suggests that the neuropeptide substance P (SP) plays a central role. The aim of this review is to examine the role of SP in ischaemic stroke and report on the potential utility of NK1 tachykinin receptor antagonists as therapeutic agents.

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Release of substance P by low oxygen in the rabbit carotid body: evidence for the involvement of calcium channels

Cited by 30 publications

References 48 publications

Gene expression in peripheral arterial chemoreceptors

Gene expression in peripheral arterial chemoreceptors

Peripheral Chemoreceptors: Function and Plasticity of the Carotid Body

The Role of Substance P in Ischaemic Brain Injury

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