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Carotid Body (carotid + body)
Selected AbstractsMorphological Investigation of Carotid Body and Its Arteries in RabbitsANATOMIA, HISTOLOGIA, EMBRYOLOGIA, Issue 5 2002E. Unur Summary The purpose of this study was to determine the morphology of the rabbit carotid body and its artery at the light microscopy level. The carotid body was situated between the internal and external carotid arteries after the bifurcation point of the common carotid artery. The carotid body was usually found to be a single, ovoid tissue mass but, in some cases it consisted of two or three parts. More carotid bodies were supplied by a single carotid body artery (glomic artery) which arose from the common carotid artery or the internal or external carotid arteries near the bifurcation point of the common carotid artery. In only one case were there two arteries which arose from opposite sides of the external carotid artery at its origin. There was a distinguishable sinus (glomic sinus) at the origin of the glomic artery. This artery had a thin wall with elastic laminae in the sinus area which become thinner distal to the sinus. [source] Neurotransmitter and neuromodulatory mechanisms at peripheral arterial chemoreceptorsEXPERIMENTAL PHYSIOLOGY, Issue 6 2010Colin A. Nurse The control of breathing depends critically on sensory inputs to the central pattern generator of the brainstem, arising from peripheral arterial chemoreceptors located principally in the carotid bodies (CBs). The CB receptors, i.e. glomus or type I cells, are excited by chemical stimuli in arterial blood, particularly hypoxia, hypercapnia, acidosis and low glucose, which initiate corrective reflex cardiorespiratory and cardiovascular adjustments. Type I cells occur in clusters and are innervated by petrosal afferent fibres. Synaptic specializations (both chemical and electrical) occur between type I cells and petrosal terminals, and between neighbouring type I cells. This, together with the presence of a wide array of neurotransmitters and neuromodulators linked to both ionotropic and metabotropic receptors, allows for a complex modulation of CB sensory output. Studies in several laboratories over the last ,20 years have provided much insight into the transduction mechanisms. More recent studies, aided by the development of a co-culture model of the rat CB, have shed light on the role of neurotransmitters and neuromodulators in shaping the afferent response. This review highlights some of these developments, which have contributed to our current understanding of information processing at CB chemoreceptors. [source] Melatonin enhances the hypoxic response of rat carotid body chemoreceptorJOURNAL OF PINEAL RESEARCH, Issue 3 2005Yueping Chen Abstract:, Melatonin attenuates carotid chemoreceptor response to hypercapnic acidosis and may contribute to the effect of circadian rhythms on the chemoreflex. The purpose of this study was to test the hypothesis that melatonin modulates rat carotid chemoreceptor response to hypoxia. To examine the effect of melatonin on the hypoxic response of the chemosensitive cells, cytosolic calcium ([Ca2+]i) was measured by spectrofluorometry in fura-2-loaded type-I (glomus) cells dissociated from rat carotid bodies. Melatonin (0.01,10 nm) did not change the resting [Ca2+]i level of the glomus cells but it concentration-dependently increased peak [Ca2+]i response to cyanide or deoxygenated buffer. An agonist of melatonin receptors, iodomelatonin also enhanced the [Ca2+]i response to hypoxia. The melatonin-induced enhancement of the [Ca2+]i response was abolished by pretreatment with nonselective mt1/MT2 antagonist, luzindole, and by MT2 antagonists, 4-phenyl-2-propionamidotetraline or DH97. These findings suggest that melatonin receptors in the glomus cells mediate the effect of melatonin on the chemoreceptor response to hypoxia. In addition, melatonin increased the carotid afferent response to hypoxia in unitary activities recorded from the sinus nerve in isolated carotid bodies superfused with bicarbonate-buffer saline. Furthermore, plethysmographic measurement of ventilatory activities in unanesthetized rats revealed that melatonin (1 mg/kg, i.p.) increased the ventilatory response to hypoxia. Hence, the circadian rhythm of melatonin in arterial blood can modulate the carotid chemoreceptor response to hypoxia. This modulation may be a physiological mechanism involved in the day-light differences in ventilatory activities. [source] Antioxidants reverse depression of the hypoxic ventilatory response by acetazolamide in manTHE JOURNAL OF PHYSIOLOGY, Issue 3 2006Luc J. Teppema The carbonic anhydrase inhibitor acetazolamide may have both inhibitory and stimulatory effects on breathing. In this placebo-controlled double-blind study we measured the effect of an intravenous dose (4 mg kg,1) of this agent on the acute isocapnic hypoxic ventilatory response in 16 healthy volunteers (haemoglobin oxygen saturation 83,85%) and examined whether its inhibitory effects on this response could be reversed by antioxidants (1 g ascorbic acid i.v. and 200 mg ,-tocopherol p.o.). The subjects were randomly divided into an antioxidant (Aox) and placebo group. In the Aox group, acetazolamide reduced the mean normocapnic and hypercapnic hypoxic responses by 37% (P < 0.01) and 55% (P < 0.01), respectively, and abolished the O2,CO2 interaction, i.e. the increase in O2 sensitivity with rising PCO2. Antioxidants completely reversed this inhibiting effect on the normocapnic hypoxic response, while in hypercapnia the reversal was partial. In the placebo group, acetazolamide reduced the normo- and hypercapnic hypoxic responses by 33 and 47%, respectively (P < 0.01 versus control in both cases), and also abolished the O2,CO2 interaction. Placebo failed to reverse these inhibitory effects of acetazolamide in this group. We hypothesize that either an isoform of carbonic anhydrase may be involved in the regulation of the redox state in the carotid bodies or that acetazolamide and antioxidants exert independent effects on oxygen-sensing cells, in which both carbonic anhydrase and potassium channels may be involved. The novel findings of this study may have clinical implications, for example with regard to a combined use of acetazolamide and antioxidants at high altitude. [source] Morphological Investigation of Carotid Body and Its Arteries in RabbitsANATOMIA, HISTOLOGIA, EMBRYOLOGIA, Issue 5 2002E. Unur Summary The purpose of this study was to determine the morphology of the rabbit carotid body and its artery at the light microscopy level. The carotid body was situated between the internal and external carotid arteries after the bifurcation point of the common carotid artery. The carotid body was usually found to be a single, ovoid tissue mass but, in some cases it consisted of two or three parts. More carotid bodies were supplied by a single carotid body artery (glomic artery) which arose from the common carotid artery or the internal or external carotid arteries near the bifurcation point of the common carotid artery. In only one case were there two arteries which arose from opposite sides of the external carotid artery at its origin. There was a distinguishable sinus (glomic sinus) at the origin of the glomic artery. This artery had a thin wall with elastic laminae in the sinus area which become thinner distal to the sinus. [source] Glucose-induced inhibition: how many ionic mechanisms?ACTA PHYSIOLOGICA, Issue 3 2010D. Burdakov Abstract Sensing of sugar by specialized ,glucose-inhibited' cells helps organisms to counteract swings in their internal energy levels. Evidence from several cell types in both vertebrates and invertebrates suggests that this process involves sugar-induced stimulation of plasma membrane K+ currents. However, the molecular composition and the mechanism of activation of the underlying channel(s) remain controversial. In mouse hypothalamic neurones and neurosecretory cells of the crab Cancer borealis, glucose stimulates K+ currents displaying leak-like properties. Yet knockout of some of the candidate ,leak' channel subunits encoded by the KCNK gene family so far failed to abolish glucose inhibition of hypothalamic cells. Moreover, in other tissues, such as the carotid body, glucose-stimulated K+ channels appear to be not leak-like but voltage-gated, suggesting that glucose-induced inhibition may engage multiple types of K+ channels. Other mechanisms of glucose-induced inhibition, such as hyperpolarization mediated by opening of Cl, channels and depolarization block caused by closure of KATP channels have also been proposed. Here we review known ionic and pharmacological features of glucose-induced inhibition in different cell types, which may help to identify its molecular correlates. [source] Expression of histamine receptors and effect of histamine in the rat carotid body chemoafferent pathwayEUROPEAN JOURNAL OF NEUROSCIENCE, Issue 12 2006Nikolai Lazarov Abstract Chemosensory information from peripheral arterial oxygen sensors in the carotid body is relayed by petrosal ganglion neurons to the respiratory networks in the medulla oblongata. Biogenic amines, including histamine, released from glomus (type I) cells of the carotid body are considered to be primary transmitters in hypoxic chemosensitivity. Immunocytochemistry at light-and electron-microscopical levels, and RT-PCR, revealed the expression of histamine receptors 1 and 3 as well as histidine decarboxylase in the rat carotid body glomus cells and petrosal ganglion neurons. Histamine receptors 1 and 3, but not histidine decarboxylase, were also observed in the ventrolateral, intermediate and commissural subnuclei of the nucleus tractus solitarii in the medulla oblongata. In order to examine the possible role of histamine in the afferent branch of the respiratory system, we applied histamine receptor 1 and 3 agonists to the carotid body, which caused a mildly increased phrenic nerve activity in a working heart,brainstem preparation. Moreover, microinjection of antagonists of histamine receptors 1 and 3 into the nucleus tractus solitarii caused significant changes in the inspiratory timing and the chemoreceptor response. Our data show that histamine acting via histamine receptors 1 and 3 plays an important neuromodulatory role in the afferent control of chemosensitivity. [source] To breathe or not to breathe?EXPERIMENTAL PHYSIOLOGY, Issue 1 2009That is the question Our understanding of the role of the brain in respiratory rhythm generation and regulation began the early nineteenth century. Over the next 150 years the neuronal groups in the medulla oblongata and pons that were involved in eupnoea and in gasping were identified by techniques involving the lesioning of areas of the lower brainstem, several transections across the brainstem and focal electrical stimulation. An incomplete picture emerged that stressed the importance of the ventral medulla. Subsequent electrophysiological studies in in vivo, in situ and in vitro preparations have revealed the importance of restricted groups of neurones in this area, within the Bötzinger and pre-Bötzinger nuclei, that are the essential kernel for rhythm generation. The outputs to the spinal motoneurones responsible for the patterning of inspiratory and expiratory discharge are shaped by inputs from these neurones and others within the respiratory complex that determine the activity of respiratory bulbospinal neurones. It is clear that the developmental stage of the preparation is often critical for the pattern of respiratory activity that is generated and that these patterns have important physiological consequences. The models that are currently considered to explain rhythmogenesis are critically evaluated. The respiratory network is subject to regulation from peripheral and central chemoreceptors, amongst other afferent inputs, which act to ensure respiratory homeostasis. The roles of peripheral chemoreceptors as primarily O2 sensors are considered, and the evolution of ideas surrounding their roles is described. New insights into the transduction mechanisms of chemoreception in the carotid body and chemosensitive areas of the ventral medullary surface, specifically in monitoring CO2 levels, are reviewed. As new experimental tools, both genetic and cellular, are emerging, it can be expected that the detailed network architecture and synaptic interactions that pattern respiratory activity in relation to behavioural activity will be revealed over the next years. [source] Definitive radiotherapy in the management of chemodectomas arising in the temporal bone, carotid body, and glomus vagaleHEAD & NECK: JOURNAL FOR THE SCIENCES & SPECIALTIES OF THE HEAD AND NECK, Issue 5 2001Russell W. Hinerman MD Abstract Purpose To evaluate the results of treatment for 71 patients with 80 chemodectomas of the temporal bone, carotid body, or glomus vagale who were treated with radiation therapy (RT) alone (72 tumors in 71 patients) or subtotal resection and RT (8 tumors) at the University of Florida between 1968 and 1998. Methods and Materials Sixty-six lesions were previously untreated, whereas 14 had undergone prior treatment (surgery, 11 lesions; RT, 1 lesion; or both, 2 lesions) and were treated for locally recurrent disease. All three patients who received prior RT had been treated at other institutions. Patients had minimum follow-up times as follows: 2 years, 66 patients (93%); 5 years, 53 patients (75%); 10 years, 37 patients (52%); 15 years, 29 patients (41%); 20 years, 18 patients (25%); 25 years, 12 patients (17%); and 30 years, 4 patients (6%). Results There were five local recurrences at 2.6 years, 4.6 years, 5.3 years, 8.3 years, and 18.8 years, respectively. Four were in glomus jugulare tumors and one was a carotid body tumor. Two of the four patients with glomus jugulare failures were salvaged, one with stereotactic radiosurgery and one with surgery and postoperative RT at another institution. Two of the five recurrences had been treated previously at other institutions with RT and/or surgery. Treatment for a third recurrence was discontinued, against medical advice, before receiving the prescribed dose. There were, therefore, only 2 failures in 65 previously untreated lesions receiving the prescribed course of RT. The overall crude local control rate for all 80 lesions was 94%, with an ultimate local control rate of 96% after salvage treatment. The incidence of treatment-related complications was low. Conclusions Irradiation offers a high probability of tumor control with relatively minimal risks for patients with chemodectomas of the temporal bone and neck. There were no severe treatment complications. © 2001 John Wiley & Sons, Inc. Head Neck 23: 363,371, 2001. [source] Caffeine inhibition of rat carotid body chemoreceptors is mediated by A2A and A2B adenosine receptorsJOURNAL OF NEUROCHEMISTRY, Issue 2 2006S. V. Conde Abstract Caffeine, an unspecific antagonist of adenosine receptors, is commonly used to treat the apnea of prematurity. We have defined the effects of caffeine on the carotid body (CB) chemoreceptors, the main peripheral controllers of breathing, and identified the adenosine receptors involved. Caffeine inhibited basal (IC50, 210 µm) and low intensity (PO2 , 66 mm Hg/30 mm K+) stimulation-induced release of catecholamines from chemoreceptor cells in intact preparations of rat CB in vitro. Opposite to caffeine, 5,-(N -ethylcarboxamido)adenosine (NECA; an A2 agonist) augmented basal and low-intensity hypoxia-induced release. 2- p -(2-Carboxyethyl)phenethyl-amino-5,- N -ethylcaboxamido-adenosine hydrochloride (CGS21680), 2-hexynyl-NECA (HE-NECA) and SCH58621 (A2A receptors agents) neither affected catecholamine release nor altered the caffeine effects. The 8-cycle-1,3-dipropylxanthine (DPCPX; an A1/A2B antagonist) and 8-(4-{[(4-cyanophenyl)carbamoylmethyl]-oxy}phenyl)-1,3-di(n-propyl)xanthine (MRS1754; an A2B antagonist) mimicking of caffeine indicated that caffeine effects are mediated by A2B receptors. Immunocytochemical A2B receptors were located in tyrosine hydroxylase positive chemoreceptor cells. Caffeine reduced by 52% the chemosensory discharges elicited by hypoxia in the carotid sinus nerve. Inhibition had two components with pharmacological analysis indicating that A2A and A2B receptors mediate, respectively, the low (17 × 10,9 m) and high (160 × 10,6 m) IC50 effects. It is concluded that endogenous adenosine, via presynaptic A2B and postsynaptic A2A receptors, can exert excitatory effects on the overall output of the rat CB chemoreceptors. [source] Gene expression in peripheral arterial chemoreceptorsMICROSCOPY RESEARCH AND TECHNIQUE, Issue 3 2002Estelle B. Gauda Abstract 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. Microsc. Res. Tech. 59:153,167, 2002. © 2002 Wiley-Liss, Inc. [source] Chronic hypoxia-induced morphological and neurochemical changes in the carotid bodyMICROSCOPY RESEARCH AND TECHNIQUE, Issue 3 2002Zun-Yi Wang Abstract The carotid body (CB) plays an important role in the control of ventilation. Type I cells in CB are considered to be the chemoreceptive element which detects the levels of PO2, PCO2, and [H+] in the arterial blood. These cells originate from the neural crest and appear to retain some neuronal properties. They are excitable and produce a number of neurochemicals. Some of these neurochemicals, such as dopamine and norepinephrine, are considered to be primarily inhibitory to CB function and others, such as adenosine triphosphate, acetylcholine, and endothelin, are thought to be primarily excitatory. Chronic hypoxia (CH) induces profound morphological as well as neurochemical changes in the CB. CH enlarges the size of CB and causes hypertrophy and mitosis of type I cells. Also, CH changes the vascular structure of CB, including inducing marked vasodilation and the growth of new blood vessels. Moreover, CH upregulates certain neurochemical systems within the CB, e.g., tyrosine hydroxylase and dopaminergic activity in type I cells. There is also evidence that CH induces neurochemical changes within the innervation of the CB, e.g., nitric oxide synthase. During CH the sensitivity of the CB chemoreceptors to hypoxia is increased but the mechanisms by which the many CH-induced structural and neurochemical changes affect the sensitivity of CB to hypoxia remains to be established. Microsc. Res. Tech. 59:168,177, 2002. © 2002 Wiley-Liss, Inc. [source] Regulation of gene expression for neurotransmitters during adaptation to hypoxia in oxygen-sensitive neuroendocrine cellsMICROSCOPY RESEARCH AND TECHNIQUE, Issue 3 2002Waltke R. Paulding Abstract Reduced oxygen tension (hypoxia) in the environment stimulates oxygen-sensitive cells in the carotid body (CB). Upon exposure to hypoxia, the CB immediately triggers a reflexive physiological response, thereby increasing respiration. Adaptation to hypoxia involves changes in the expression of various CB genes, whose products are involved in the transduction and modulation of the hypoxic signal to the central nervous system (CNS). Genes encoding neurotransmitter-synthesizing enzymes and receptors are particularly important in this regard. The cellular response to hypoxia correlates closely with the release and biosynthesis of catecholamines. The gene expression of tyrosine hydroxylase (TH), the rate-limiting enzyme for catecholamine biosynthesis, is regulated by hypoxia in the CB and in the oxygen-sensitive cultured PC12 cell line. Recently, genomic microarray studies have identified additional genes regulated by hypoxia. Patterns of gene expression vary, depending on the type of applied hypoxia, e.g., intermittent vs. chronic. Construction of a hypoxia-regulated, CB-specific, subtractive cDNA library will enable us to further characterize regulation of gene expression in the CB. Microsc. Res. Tech. 59:178,187, 2002. © 2002 Wiley-Liss, Inc. [source] Peripheral chemoreceptors determine the respiratory sensitivity of central chemoreceptors to CO2THE JOURNAL OF PHYSIOLOGY, Issue 13 2010Gregory M. Blain We assessed the contribution of carotid body chemoreceptors to the ventilatory response to specific CNS hypercapnia in eight unanaesthetized, awake dogs. We denervated one carotid body (CB) and used extracorporeal blood perfusion of the reversibly isolated remaining CB to maintain normal CB blood gases (normoxic, normocapnic perfusate), to inhibit (hyperoxic, hypocapnic perfusate) or to stimulate (hypoxic, normocapnic perfusate) the CB chemoreflex, while the systemic circulation, and therefore the CNS and central chemoreceptors, were exposed consecutively to four progressive levels of systemic arterial hypercapnia via increased fractional inspired CO2 for 7 min at each level. Neither unilateral CB denervation nor CB perfusion, per se, affected breathing. Relative to CB control conditions (normoxic, normocapnic perfusion), we found that CB chemoreflex inhibition decreased the slope of the ventilatory response to CNS hypercapnia in all dogs to an average of 19% of control values (range 0,38%; n= 6), whereas CB chemoreflex stimulation increased the slope of the ventilatory response to CNS hypercapnia in all dogs to an average of 223% of control values (range 204,235%; n= 4). We conclude that the gain of the CNS CO2/H+ chemoreceptors in dogs is critically dependent on CB afferent activity and that CNS,CB interaction results in hyperadditive ventilatory responses to central hypercapnia. [source] Morphological Investigation of Carotid Body and Its Arteries in RabbitsANATOMIA, HISTOLOGIA, EMBRYOLOGIA, Issue 5 2002E. Unur Summary The purpose of this study was to determine the morphology of the rabbit carotid body and its artery at the light microscopy level. The carotid body was situated between the internal and external carotid arteries after the bifurcation point of the common carotid artery. The carotid body was usually found to be a single, ovoid tissue mass but, in some cases it consisted of two or three parts. More carotid bodies were supplied by a single carotid body artery (glomic artery) which arose from the common carotid artery or the internal or external carotid arteries near the bifurcation point of the common carotid artery. In only one case were there two arteries which arose from opposite sides of the external carotid artery at its origin. There was a distinguishable sinus (glomic sinus) at the origin of the glomic artery. This artery had a thin wall with elastic laminae in the sinus area which become thinner distal to the sinus. [source] SDHC mutation in an elderly patient without familial antecedentsCLINICAL ENDOCRINOLOGY, Issue 6 2008Elena López-Jiménez Summary Head and neck paragangliomas are usually asymptomatic and benign tumours arising mainly from the carotid body and the vagal, tympanic or jugular glomus. The majority of patients develop sporadic masses, and around 30% of cases harbour germline mutations in one of the succinate dehydrogenase genes: SDHB, SDHC or SDHD. In these hereditary cases, the presence of familial antecedents of the disease, multiplicity/bilaterality, young age at onset, and more recently, presence of gastrointestinal stromal tumours, are main factors to be considered. Here we describe a new mutation (c.256,257insTTT) affecting the SDHC gene in a 60-year-old-patient with a single head and neck paraganglioma, and without familial antecedents of the disease. In silico splice site analysis showed that this variant created a cryptic splice acceptor site and loss of heterozygosity (LOH) supported the pathogenic role of the mutation. Control population analyses did not detect this variant but revealed a novel SDHC polymorphism that exhibited a frequency of 0·3% (3/1020). This latter finding highlights the importance of assessing the clinical relevance of variants of unknown significance by means of analysing sufficient controls. Despite having found a germline mutation in an older, apparently sporadic patient, we consider that the high costs of analysing all susceptibility genes related to the disease support the recommendation of screening for mutations only in patients fulfilling the above criteria. [source] | |||||||||||||||||||||||||