Disease relevance of Carotid Body

• Here we show that low glucose increases secretion from glomus cells in the carotid bodies, sensory organs whose stimulation by hypoxia produces sympathetic activation, by a process that depends on extracellular Ca2+ influx and is paralleled by inhibition of voltage-gated K+ channels [1].
• Sudden infant death syndrome: increased carotid-body dopamine and noradrenaline content [2].
• Migraine, serotonin, and the carotid body [3].
• The carotid bodies are sensitive to glucose in vitro and can be stimulated to cause hyperglycemia in vivo [4].
• In addition, we found that hypercapnia, another natural stimulus of carotid body activity, failed to enhance TH mRNA in type I cells [5].

High impact information on Carotid Body

• Enkephalin-, VIP- and substance P-like immunoreactivity in the carotid body [6].
• Met- and Leu-enkephalin-like material occurred in considerable quantities in carotid body extracts and enkephalin-like immunoreactivity was localised in type I cells [6].
• In glomus cells of the carotid body, the differential properties of O2-sensitive K+ and Ca2+ channels help us to understand the basic features of O2 chemoreception [7].
• Low glucose-sensing cells in the carotid body [1].
• We have tested the suitability of chromaffin-like carotid body glomus cells for dopamine cell replacement in Parkinsonian rats [8].

Chemical compound and disease context of Carotid Body

• Normally, O2-sensitive K+ channels in neurosecretory type I carotid body cells are intimately involved in excitation of the intact organ by hypoxia [9].
• In in vivo studies, close carotid body (intraarterial) administration of CP-96,345 attenuated the sensory response to hypoxia in a dose-dependent manner with 73% of the response abolished at doses of 0.3-0.6 mg/kg [10].
• Secretory responses of intact glomus cells in thin slices of rat carotid body to hypoxia and tetraethylammonium [11].
• 2. Prenatal hypoxia decreased the dopamine content in the carotid bodies at all ages, and decreased the utilisation rate of noradrenaline in the caudal part of the A2 (A2c), A1 and A5 noradrenergic brainstem cell groups at 3 weeks after birth [12].
• 6. Our results show that the neonatal lamb possesses a carotid body steady-state CO2 sensitivity within a few days of birth, an age when hypoxia sensitivity is low [13].

Biological context of Carotid Body

• In CIH animals, carotid body complex I activity of the mitochondrial electron transport is inhibited, suggesting mitochondria as one source of O2.- generation [14].
• Regulation of tyrosine hydroxylase gene expression in the rat carotid body by hypoxia [15].
• In 12 cats, this activity was measured during inhalation of an hypoxic gas mixture with halothane, 0, 0.1, and 0.8%, with intact or denervated carotid bodies [16].
• Tyrosine hydroxylase- and substance P-positive neurons constitute separate subpopulations of carotid body afferents, as these two phenotypes were not colocalized [17].
• The goal of the present study was to determine whether carotid body glomus cells express HERG-like K(+) current, and if so, to determine whether a HERG-like current regulates the resting membrane potential [18].

Anatomical context of Carotid Body

• Integration of our own morphological observations into recent ultrastructural, biochemical, and neuropharmacological results on the carotid body led to a new hypothesis on chemoreceptor function: (i) Glomus cells with small dense-cored vesicles (type IB cells) that store norepinephrine are chemoreceptors [19].
• The rapid response to hypoxia in the pulmonary artery (PA), carotid body, and ductus arteriosus is partially mediated by O2-responsive K+ channels [20].
• The superior cervical ganglion rather showed hypertrophic features in Hoxa3 homozygous mutants lacking the carotid body [21].
• All the mammalian dopamine receptors, initially cloned from the brain, have been found to be expressed outside the central nervous system, in such sites as the adrenal gland, blood vessels, carotid body, intestines, heart, parathyroid gland, and the kidney and urinary tract [22].
• Thus, the present study evidenced that the absence of the carotid body in Hoxa3 homozygous mutants is due to the defect of development of the third arch artery, resulting in malformation of the carotid artery system [21].

Associations of Carotid Body with chemical compounds

• Carotid bodies are sensory organs for monitoring arterial oxygen and CO2 [10].
• Carbon monoxide: a role in carotid body chemoreception [23].
• In the present study, we examined the physiological importance of SP in carotid body chemoreception by using a selective nonpeptide SP [neurokinin (NK) 1] receptor antagonist CP-96,345 [10].
• (c) Once oxygen is sensed and Ca(2+) is released, the neurotransmittesr will be elaborated from the glomus cells of the carotid body [24].
• In this review, we will examine recent evidence supporting the notion that acetylcholine and adenosine 5'-triphosphate are the main excitatory transmitters in the cat and rat carotid bodies [25].

Gene context of Carotid Body

• Histologic analysis revealed no abnormalities of carotid body morphology in Hif1a(+/-) mice [26].
• We found that Hoxa3 homozygous null mutant mice had the lack of the carotid body [21].
• However, in the absence of target tissues, a large proportion of carotid body afferents could be rescued by implants containing BDNF [27].
• Mash1 is required for glomus cell formation in the mouse carotid body [28].
• In summary, our results suggest that Epo controls ventilation at the central (brainstem) and peripheral (carotid body) levels [29].

Analytical, diagnostic and therapeutic context of Carotid Body

• Chronic (15 days) carotid sinus nerve denervation or superior cervical ganglionectomy did not modify the carotid body dopamine content (5-6 nmol/mg of protein, equivalent to 250 pmol per carotid body), but sympathectomy reduced by approximately 50% the norepinephrine content [30].
• In situ hybridization study with antisense mt1 and MT2 receptor mRNA oligonucleotide probes showed an expression of mt1 and MT2 receptors in the rat carotid body [31].
• HPLC identification of opioid peptides revealed that the sequences of Met- and Leu-enkephalin were in a proportion of nearly 6:1, indicating that the main opioid precursor in the carotid body is proenkephalin A [30].
• 1. A high density of angiotensin II receptors was observed in the rat carotid body by in vitro autoradiography employing 125I-[Sar1, Ile8]-angiotensin II as radioligand [32].
• Acetylcholine content of normal and denervated cat carotid bodies measured by pyrolysis gas chromatography/mass fragmentometry [33].

References