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At least 289 records · Page 16Linked to original sources
PubMed2006

Expression of multiple P2X receptors by glossopharyngeal neurons projecting to rat carotid body O2-chemoreceptors: role in nitric oxide-mediated efferent inhibition.

In mammals, ventilation is peripherally controlled by the carotid body (CB), which receives afferent innervation from the petrosal ganglion and efferent innervation from neurons located along the glossopharyngeal nerve (GPN). GPN neurons give rise to the "efferent inhibitory" pathway via a plexus of neuronal nitric oxide (NO) synthase-positive fibers, believed to be responsible for CB chemoreceptor inhibition via NO release. Although NO is elevated during natural CB stimulation by hypoxia, the underlying mechanisms are unclear. We hypothesized that ATP, released by rat CB chemoreceptors (type 1 cells) and/or red blood cells during hypoxia, may directly activate GPN neurons and contribute to NO-mediated inhibition. Using combined electrophysiological, molecular, and confocal immunofluorescence techniques, we detected the expression of multiple P2X receptors in GPN neurons. These receptors involve at least four different purinergic subunits: P2X2 [and the splice variant P2X2(b)], P2X3, P2X4, and P2X7. Using a novel coculture preparation of CB type I cell clusters and GPN neurons, we tested the role of P2X signaling on CB function. In cocultures, fast application of ATP, or its synthetic analog 2',3'-O-(4 benzoylbenzoyl)-ATP, caused type I cell hyperpolarization that was prevented in the presence of the NO scavenger 2-(4-carboxyphenyl)-4,4,5,5-tetramethyl-imidazoline-1-oxyl-3-oxide potassium. These data suggest that ATP released during hypoxic stress from CB chemoreceptors (and/or red blood cells) will cause GPN neuron depolarization mediated by multiple P2X receptors. Activation of this pathway will lead to calcium influx and efferent inhibition of CB chemoreceptors via NO synthesis and consequent release.

Adenosine Triphosphate↗
PubMed2006

Purinergic P2 receptors modulate excitability but do not mediate pH sensitivity of RTN respiratory chemoreceptors.

The cellular mechanism(s) by which the brain senses changes in pH to regulate breathing (i.e., central chemoreception) have remained incompletely understood, in large part because the central respiratory chemoreceptors have themselves eluded detection. Here, we recorded from a newly identified population of central chemoreceptors located in the retrotrapezoid nucleus (RTN) on the ventral surface of the brainstem to test a recently proposed role for purinergic P2 receptor signaling in central respiratory chemoreception (Gourine et al., 2005). Using loose-patch current-clamp recordings in brainstem slices from rat pups (postnatal day 7-12), we indeed show purinergic modulation of pH-sensitive RTN neurons: activation of P2X receptors indirectly inhibited RTN firing by increasing inhibitory input, whereas P2Y receptor stimulation caused direct excitation of RTN chemoreceptors. However, after blocking P2 receptors with the broad-spectrum antagonists PPADS (pyridoxal-phosphate-6-azophenyl-2',4'-disulfonate) or RB2 (reactive blue 2), the pH sensitivity of RTN neurons remained intact. Therefore, we conclude that purinergic signaling can modulate RTN neuron activity but does not mediate the pH sensing intrinsic to these central respiratory chemoreceptors.

Adenosine Triphosphate↗
PubMed1981

Alteration of chemoreceptor responses and ultrastructural features of ischemic carotid body of the cat.

Effects of short-term ischemia on chemoreceptor responses to various stimuli and ultrastructural features of the carotid body of the cat were examined. Total occlusion of the arteries supplying the carotid body induced an increase in chemoreceptor discharges. After 1-hr ischemia, chemoreceptor responses to NaCN and asphyxia were markedly depressed to 10-40% of the control, while those to ACh and HCl were not greatly affected. Prolonged ischemia (2-3 hr) produced a marked decrease in responsiveness to all stimuli. One-hr ischemia induced changes in the ultrastructural appearance of the glomus cell, including a decrease in the number of dense-cored vesicles, the appearance of swollen or vacuolated mitochondria and amorphous substances, while the nerve ending showed a relatively well-preserved appearance. Prolonged ischemia (2-3 hr) produced degenerative changes both in the glomus cell and nerve ending; vacuolation, a marked decrease in electron density of cytoplasmic matrix of the glomus cell and nerve ending, and marginal shrinkage of the nuclei. The results indicate that the markedly depressed responses to NaCN and asphyxia after 1-hr ischemia are due to dysfunction of the glomus cell, while ACh and HCl, acting directly on the nerve ending which was not greatly affected by ischemia, evoked well-preserved responses in the chemoreceptors.

Animals↗
PubMed1991

Influences of lung mechanoreceptors and carotid chemoreceptors on the response of respiratory muscle activity to tracheal occlusion.

We examined the responses of respiratory muscle electromyograms (EMGs) from internal (IIC) and external intercostal (EIC) muscles and diaphragm (DIAP) to three successive occluded breaths in anesthetized spontaneously breathing rabbits. Both inspiratory and expiratory muscle EMGs progressively increased in the course of tracheal occlusion. An increase in these muscle EMGs was still observed after release of tracheal occlusion, but those effects were short-lasting. In a separate series of experiments, for assessment of possible reflex effects involved, the responses of slowly adapting pulmonary stretch receptor (SAR), rapidly adapting pulmonary stretch receptor (RAR), and carotid chemoreceptor activities to tracheal occlusion lasting for three respiratory efforts were also examined. The inspiratory discharge of SARs decreased but the expiratory discharge of SARs increased during tracheal occlusion. Although carotid chemoreceptors increased their activity in the latency of 3-6s after the onset of tracheal occlusion, the activity of RARs was greatly reduced throughout the period of tracheal occlusion. A transient increase in both carotid chemoreceptors and RARs was still observed after release of tracheal occlusion. These results suggest that alterations of inspiratory and expiratory muscle EMGs produced by tracheal occlusion would appear to be mediated by the afferent inputs from lung mechanoreceptors and carotid chemoreceptors.

Animals↗
PubMed1997

Excitatory amino acid receptors in the paraventricular hypothalamic nucleus mediate pressor response induced by carotid body chemoreceptor stimulation in rats.

In urethane-anesthetized rats with spinal transection, antagonists of excitatory amino acid receptors, P2 purinoceptors and adrenoceptors were microinjected into the paraventricular hypothalamic nucleus (PVN) and their effects on the pressor response evoked by carotid body chemoreceptor stimulation were examined. Microinjections of the non-selective excitatory amino acid antagonist kynurenate, the non-NMDA receptor antagonist CNQX and the NMDA antagonist 2-amino-5-phosphonovalerate (AP5) into the PVN inhibited the chemoreceptor reflex-induced pressor response. The excitatory amino acid agonist L-glutamate injected into the PVN produced an increase in blood pressure. The P2 purinoceptor antagonist suramin did not affect the pressor response and ATP did not affect basal blood pressure. The alpha adrenoceptor antagonist phentolamine, prazosin and yohimbine also inhibited the chemoreceptor-induced pressor response, while the beta antagonist propranolol did not affect it. These findings indicate that excitatory amino acid receptors and alpha adrenoceptors in the PVN are involved in mediating the pressor response induced by carotid body chemoreceptor stimulation in rats.

2-Amino-5-phosphonovalerate↗
PubMed1991

Peripheral chemoreceptor reflex in obstructive sleep apnea patients; a relationship between ventilatory response to hypoxia and nocturnal bradycardia during apnea events.

15 patients with obstructive sleep apnea syndrome and arterial hypertension (H-OSAS), 25 normotensive patients with sleep apnea syndrome (N-OSAS) and 20 healthy age-matched controls (C) were included in this study. Ventilatory responses to activation (hypoxia) and inactivation (hyperoxia) of carotid chemoreceptors were studied in all subjects. Relationship between hypoxic ventilatory reactivity and nocturnal bradycardia during apnea-phases was analysed in both groups of patients. Results and conclusions. 1. We found an impairment of ventilatory response to hypoxia in H-OSAS and N-OSAS patients. However, the increase in ventilation in response to hypoxia was significantly greater in H-OSAS as compared to N-OSAS patients. 2. An augmented ventilatory response to inactivation of carotid chemoreceptors (the decrease in ventilation), observed in H-OSAS patients, indicates an increase in resting peripheral chemoreceptors drive in this group of patients. 3. The relationship between ventilatory response to hypoxia and nocturnal bradycaria in obstructive sleep apnea patients suggests, that hypoxic reactivity of arterial chemoreceptors might be involved in the origin of bradycardia during apnea events.

Bradycardia↗
PubMed1985

[The autonomous nervous system and pulmonary circulation. Stimulation of chemoreceptors and ventilation/perfusion ratios].

The existence of neurogenic pulmonary vasomotrocity and of vasomotor reflexes elicited by stimulation of peripheral chemoreceptors has been demonstrated in different animal species. There are efferent noradrenergic and cholinergic nerve endings in the walls of musculo-pulmonary arteries. Stimulation of sympathetic efferents and exogenous noradrenaline cause vasoconstriction of pulmonary arteries when initial vasomotor tone is normal. There are also beta-adrenergic and cholinergic vasodilation pathways whose effects oppose the above mentioned vasoconstrictor ones, are blocked by the corresponding inhibitors, and can be demonstrated when initial vasomotor tone is high. The role of pulmonary vasomotor tone in the distribution of ventilation perfusion ratios is unknown. The stimulation of peripheral chemoreceptors causes a rise in pulmonary vascular resistance. Inversely, the stimulation of peripheral chemoreceptors by hypoxia prevents the local vasoconstrictor effect of localised alveolar hypoxia in sheep. There are thus theoretical reasons to think that the effect on regional pulmonary resistance of nervous stimulation may differ in cases of inhomogeneous lung disease, according to the local state of the pulmonary vessels. Consequently, it is not possible to anticipate the effect of stimulating chemoreceptors on the distribution of ventilation/perfusion ratios.

Animals↗
PubMed1987

Influence of chemoreceptors on neurohypophyseal blood flow during hypoxic hypoxia.

Neurohypophyseal blood flow was studied using radiolabelled microspheres in 13 dogs. Hypoxic hypoxia and carbon monoxide hypoxia with similar arterial oxygen contents (CaO2, approximately 8 vol %) were produced. Under conditions of hypoxic hypoxia, 100-200% increases in blood flow in caudate nucleus, white matter, neurohypophysis, and all other brain regions occurred. Similar blood flow responses were observed with carbon monoxide hypoxia in all brain regions except the neurohypophysis. The role of carotid and aortic chemoreceptors in mediating this blood flow response was studied in 6 additional dogs. Similar degrees of hypoxic hypoxia were produced in chemoreceptor-intact and completely denervated animals (CaO2 approximately 8 vol %, PaO2 approximately 33 mm Hg). Hypoxic hypoxia produced a 250% increase in neurohypophyseal blood flow and a concurrent rise in plasma arginine vasopressin from 8 +/- 3 to 52 +/- 8 pg/ml. Chemoreceptor denervation completely inhibited the increase in neurohypophyseal blood flow associated with hypoxic hypoxia. Arginine vasopressin was not increased by hypoxic hypoxia under conditions of complete denervation. A unique role for peripheral chemoreceptors in regulating neurohypophyseal blood flow is postulated.

Animals↗
PubMed1980

Regulation of chemoreceptor sensitivity in the carotid body: the role of presynaptic sensory nerves.

Several neural and vascular mechanisms regulate the sensitivity of carotid body chemoreceptors to hypoxia, hypercapnia, and acidosis. Factors that control blood flow and oxygen delivery in the carotid body along with those that augment or diminish catecholamine release from glomus cells can have major effects on chemoreceptor function. In addition, the sensory nerves themselves may participate in the regulation of chemoreceptor sensitivity. A portion of the carotid body's sensory nerves are presynaptic to glomus cells. In response to stimulation, the sensory nerve terminals exhibit ultrastructural changes that resemble changes associated with increased release of transmitter from motor nerves: 1) the number of small (synaptic) vesicles decreases; and 2) coated vesicles and coated regions of cisternal membrane increase in number during stimulation. If sensory nerves of the carotid body release a neurotransmitters, sensory nerve activity could influence glomus cell secretion of catecholamines or other substances tha modify chemoreceptor sensitivity. Such an effect could be produced in the carotid body by hypoxia and other conditions that stimulate the sensory nerves or it could result from antidromic activity evoked in the sensory nerves by primary afferent depolarization of their terminals in the CNS.

Animals↗
PubMed1980

Site of termination of primary afferents from the carotid body chemoreceptors.

The precise site of termination of primary afferents from the carotid chemoreceptors, has not been revealed as yet by anatomical or physiological studies. Identified units in the dorsal and ventral respiratory groups in the medulla can be evoked by chemoreceptor stimulation during inspiration, and inhibited by stimulation during expiration. Thus chemoreceptor input appears to be gated by an unidentified population of respiratory units before it reaches the recognized populations. For this as well as other reasons, we propose that chemoreceptor fibers terminate on a population of small interneurons that are the pattern generators for respiratory rhythmicity. At least two paired pattern generators exist, one pair associated with the dorsal respiratory group, and a second pair associated with the ventral respiratory group.

Afferent Pathways↗
PubMed1977

Effects of carotid chemoreceptor and baroreceptor stimulation upon the sympathetic preganglionic and postganglionic cardiac nerve and single fiber activity in cats.

The stimulation of arterial baroreceptors (blind sack technique) inhibited the preganglionic and postganglionic cardiac sympathetic activity. There were found three populations of single sympathetic preganglionic fibers (Th3) responding in a different way to the stimulation of arterial baroreceptors and arterial chemoreceptors (infusion of the small volume of saline bubbled with CO2 into the carotid sinus): (i) inhibited by carotid baroreceptors and excited by carotid chemoreceptors stimulation, (ii) inhibited by carotid baroreceptors and by carotid chemoreceptors stimulation, (iii) some fibers inhibited by baroreceptors did not change activity during stimulation of chemoreceptors. A functional role of each particular group of preganglionic sympathetic fibers is discussed.

Action Potentials↗
PubMed1996

AMPA/kainate receptors mediate sympathetic chemoreceptor reflex in the rostral ventrolateral medulla.

Previous studies have reported that information from carotid chemoreceptors activates sympathetic premotor neurons in the rostral ventrolateral medulla (RVLM) exclusively via N-methyl-D-aspartic acid (NMDA) receptors. In this study, we examined the possible involvement of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)/kainate receptors in the RVLM on sympathetic chemoreceptor reflex in pentobarbitone anaesthetised, vagotomised and artificially ventilated rats. Carotid chemoreceptor stimulation with brief N2 inhalation increased splanchnic sympathetic nerve activity and arterial pressure in animals that had received an intravenous injection of the non-competitive NMDA receptor blocker, MK-801 (2 mg/kg). RVLM sympathetic premotor neurons could also be activated by brief hypoxia in the presence of MK-801. However, microinjection of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, a selective AMPA/kainate receptor antagonist, 2 mM, 100 nl) into the RVLM after intravenous MK-801 abolished the hypoxia evoked sympathoexcitatory response. These results demonstrate that AMPA/kainate receptors in the RVLM are involved in the chemoreceptor reflex pathway.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1995

Blunted peripheral chemoreceptor response to hyperoxia in a group of infants with bronchopulmonary dysplasia.

Infants with BPD often suffer from chronic hypoxia and require supplemental oxygen (O2). This might affect the sensitivity of peripheral chemoreceptors. Therefore, we assessed peripheral chemoreceptor function in 25 infants with bronchopulmonary dysplasia (BPD) of varying severity, using the hyperoxic test. These infants were compared with 35 preterm infants who did not develop BPD. All infants were tested during the 40th week of postconceptional age and their mean postnatal age was 81.5 +/- 16.3 days. Sixty percent (15/25) of the BPD infants lacked a hyperoxic response, while the proportion of nonresponders to O2 among the other groups was 20% (7/35). The intensity of this response was negatively correlated to time spent on a ventilator and positively to time without supplemental oxygen. The intensity of chemoreceptor function was closely related to the severity of BPD; none of the infants with the most severe form of BPD (grade 3) showed a ventilatory response to hyperoxia. Furthermore, infants with BPD needed significantly longer time to increase their saturation than did non-BPD infants (4.7 and 9.3 sec, respectively). We conclude that many infants with BPD, particularly those with the most severe form of the disease, have abnormally functioning peripheral chemoreceptors.

Bronchopulmonary Dysplasia↗
PubMed1984

beta-Adrenoceptor blockade spares chemoreceptor responsiveness to hypoxia.

The effect of beta-adrenoceptor blockade on the carotid body chemoreceptor response to hypoxia was assessed in anesthetized and paralyzed cats. Propranolol, atenolol and ICI 118,551 each abolished the enhancement of chemoreceptor activity produced by i.v. infusion of exogenous isoproterenol; however, the blocking drugs did not significantly diminish the increase in chemoreceptor neural discharge induced by hypoxia. These results do not support the hypothesis that beta-adrenergic receptors play an essential role in the chemoreceptor response to oxygen deprivation.

Animals↗
PubMed1976

Role of the carotid chemoreceptors in the hyperpnea of exercise in the cat.

The role of the carotid chemoreceptors in the hyperpnea of exercise was investigated. The activity of the sinus nerve of the cat was monitored while the blood supply to the carotid body was controlled independently of the systemic circulation. By this technique, fluctuations in the arterial blood was gases during a short interval of exercise induced by electrical stimulation of hindlimb muscles were unable to affect the chemoreceptor activity. While minute ventilation increased by an average of 51%, chemoreceptor discharge was found to be unchanged in 12 experiments, 6 while perfusing with normoxic blood and 6 while perfusing with hypoxic blood. Thus, it must be concluded that alteration of carotid chemoreceptor sensitivity does not occur during artificially induced exercise in anesthetized cats. However, the difference in the time course of ventilation following the initiation of artificially induced exercise between cats and other species does not allow it to be ruled out in other species, including man. Indirect evidence is against such a role.

Animals↗
PubMed1984

Effects of carotid chemoreceptor excitation on medullary expiratory neurons in cats.

A previous report (Lipski et al., 1977, J. Physiol. (London) 269, 797-810) demonstrated an inhibition of the medullary dorsal inspiratory neurons when a phasic chemoreceptor stimulus was applied during expiration. The present study tested the response of expiratory neurons which might mediate this inhibition. Recordings were made in cats anaesthetized with chloralose-urethane from the C5 phrenic rootlet and mainly from the rostral (Bötzinger) and caudal (nucleus retroambigualis, NRA) groups of medullary expiratory neurons. Carotid chemoreceptors were excited by close arterial injections of CO2-equilibrated saline. The stimuli were applied automatically with a preset delay within the respiratory cycle. The stimuli applied in inspiration excited both the phrenic activity and ventral inspiratory neurons within less than 0.5 sec. The stimuli applied in expiration excited 17 out of 25 NRA units, none of which projected to the contralateral dorsal (NTS) respiratory group. Four out of 9 units within be responsible for the expiratory inhibition of NTS inspiratory cells produced by chemoreceptor stimulation, while the caudal expiratory neurons are involved in the mediation of the chemoreceptor-induced effects upon the spinal neurons.

Animals↗
PubMed2001

The roles of the multiple CheW and CheA homologues in chemotaxis and in chemoreceptor localization in Rhodobacter sphaeroides.

Rhodobacter sphaeroides has multiple homologues of most of the Escherichia coli chemotaxis genes, organized in two major operons and other, unlinked, loci. These include cheA1 and cheW1 (che Op1) and cheA2, cheW2 and cheW3 (che Op2). We have deleted each of these cheA and cheW homologues in-frame and examined the chemosensory behaviour of these strains on swarm plates and in tethered cell assays. In addition, we have examined the effect of these deletions on the polar localization of the chemoreceptor McpG. In E. coli, deletion of either cheA or cheW results in a non-chemotactic phenotype, and these strains also show no receptor clustering. Here, we demonstrate that CheW2 and CheA2 are required for the normal localization of McpG and for normal chemotactic responses under both aerobic and photoheterotrophic conditions. Under aerobic conditions, deletion of cheW3 has no significant effect on McpG localization and only has an effect on chemotaxis to shallow gradients in swarm plates. Under photoheterotrophic conditions, however, CheW3 is required for McpG localization and also for chemotaxis both on swarm plates and in the tethered cell assay. These phenotypes are not a direct result of delocalization of McpG, as this chemoreceptor does not mediate chemotaxis to any of the compounds tested and can therefore be considered a marker for general methyl-accepting chemotaxis protein (MCP) clustering. Thus, there is a correlation between the normal localization of McpG (and presumably other chemoreceptors) and chemotaxis. We propose a model in which the multiple different MCPs in R. sphaeroides are contained within a polar chemoreceptor cluster. Deletion of cheW2 and cheA2 under both aerobic and photoheterotrophic conditions, and cheW3 under photoheterotrophic conditions, disrupts the cluster and hence reduces chemotaxis to any compound sensed by these MCPs.

Aerobiosis↗
PubMed2003

The conserved cytoplasmic module of the transmembrane chemoreceptor McpC mediates carbohydrate chemotaxis in Bacillus subtilis.

Escherichia coli cells use two distinct sensory circuits during chemotaxis towards carbohydrates. One circuit requires the phosphoenolpyruvate-dependent phosphotransferase system (PTS) and is independent of any specific chemoreceptor, whereas the other uses a chemoreceptor-dependent sensory mechanism analogous to that used during chemotaxis towards amino acids. Work on the carbohydrate chemotaxis sensory circuit of Bacillus subtilis reported in this article indicates that the B. subtilis circuit is different from either of those used by E. coli. Our chemotactic analysis of B. subtilis strains expressing various chimeric chemoreceptors indicates that the cytoplasmic, C-terminal module of the chemoreceptor McpC acts as a sensory-input element during carbohydrate chemotaxis. Our results also indicate that PTS-mediated carbohydrate transport, but not carbohydrate metabolism, is required for production of a chemotactic signal. We propose a model in which PTS-transport-induced chemotactic signals are transmitted to the C-terminal module of McpC for control of chemotaxis towards PTS carbohydrates.

Bacillus subtilis↗