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PubMed1992

Inhibition of arterial baroreceptor and chemoreceptor reflex responses by neuropeptide Y in anaesthetised dogs.

The effects of bolus intravenous injections of neuropeptide Y (NPY) on increases in pulse interval (PI) evoked reflexly by arterial chemoreceptor and baroreceptor stimulation were investigated in anaesthetised dogs. The arterial chemoreceptors were stimulated by rapid injections of small volumes of CO2 into the carotid sinus or brief episodes of tracheal occlusion. Intravenous injections of NPY produced a prolonged attenuation of the reflex prolongation of PI induced by both methods. Two methods of testing the arterial baroreceptor reflex were used: steady-state increases in PI evoked in response to maintained step increases in systolic arterial blood pressure (SABP) from inflation of an aortic balloon-tipped catheter, and beat-by-beat increases in PI evoked reflexly by 'ramp' increases in blood pressure caused by intravenous injections of phenylephrine. In both methods the relationship between SABP and PI is linear over the range tested (up to SABP 200 mmHg), the slope of the line indicating the sensitivity of the reflex response. Intravenous injections of NPY produced a prolonged attenuation of the baroreceptor-cardiodepressor reflex measured by both methods. No significant differences were observed between the NPY-mediated inhibition of the direct effects on PI of electrical stimulation of a vagus nerve, and its inhibition of the reflex responses of PI to chemoreceptor or baroreceptor stimulation. The results indicate that the attenuation of reflex PI responses to arterial chemoreceptor and baroreceptor stimulation following an intravenous injection of NPY can be accounted for in terms of the action of NPY on vagal nerve endings at the heart, although additional sites of action cannot be ruled out.

Anesthesia↗

PubMed1995

Inhibition of nitric oxide synthesis potentiates the responsiveness of carotid chemoreceptors to systemic hypoxia in the rat.

Carotid sinus nerve afferent activity was recorded in the peripheral end of the cut carotid sinus nerves in rats anesthetized with urethane, paralyzed and artificially ventilated with pure oxygen in order to abolish any resting chemoreceptor activity. Hypoxic stimuli were applied by switching pure oxygen to a nitrogen/oxygen gas mixture in the inspiratory line, reducing end-tidal oxygen concentrations to 10% FETO2, 8% FETO2 and 6% FETO2 respectively. Each stimulus was applied for 60 s and ventilation was switched again to pure oxygen. Increases in the carotid sinus nerve activities were due to chemo- and not to baroreceptor stimulation as arterial blood pressure decreased during hypoxia. After administration of nitric oxide synthase blocker L-NG-nitroarginine methyl ester, 30 mg/kg weight i.v., chemoreceptor excitatory response to all hypoxic stimuli increased significantly. Subsequent administration of L-arginine, 300 mg/kg weight i.v., restored chemoreceptor response to hypoxia to initial magnitude. It is concluded that NO is generated in the carotid body and attenuates chemoreceptor responsiveness in rats in vivo, as reported on isolated carotid bodies in cats in vitro.

Afferent Pathways↗

PubMed1986

Carotid chemoreceptor reflex in rats during experimental tetanus toxicity.

The effects of stimulation of carotid body chemoreceptors on blood pressure, heart rate and ventilation were compared in normal rats and rats with local or generalised tetanus toxicity induced by injection of the toxin. Carotid chemoreceptor stimulation in an increase in blood pressure and a decrease in heart rate in both control and tetanus rats. However, while chemoreceptor stimulation resulted in increases in ventilation of 115% and 123% in normal rats and rats with local tetanus respectively, the increase in rats with generalised tetanus was only 29%. The experiments indicate that normal rats and rats with tetanus toxicity exhibit identical pressor and heart rate responses to stimulation of carotid chemoreceptors whereas the ventilatory response is attenuated in the tetanus rats.

Animals↗

PubMed1996

Comparison of neurons in rat medulla oblongata with fos immunoreactivity evoked by seizures, chemoreceptor, or baroreceptor stimulation.

Neurons in rat medulla oblongata with Fos immunoreactivity as a marker of synaptic excitation evoked by pentylenetetrazole-induced seizures were compared with cell populations activated by the stimulation of chemoreceptor and baroreceptor afferent pathways. Chemoreceptors were stimulated by placing rats in a hypoxic gas mixture (7% oxygen) for 2 h. Baroreceptors were activated by phenylephrine-induced hypertension. Seizures and hypoxia induced Fos immunoreactivity in neurons with similar anatomical distributions in the nucleus tractus solitarius, dorsal motor nucleus of the vagus, and ventrolateral medulla. Hypertension was associated with Fos immunoreactivity in an overlapping anatomical distribution compared to seizures and hypoxia, but in a more restricted pattern. A similar proportion of catecholaminergic cells of medulla oblongata (cells immunoreactive for catecholamine synthetic enzymes, tyrosine hydroxylase or phenylethanolamine-N-methyltransferase) had Fos immunostaining after seizures and hypoxia (P > 0.05), while significantly fewer were activated by hypertension (P < 0.05). The majority of tyrosine hydroxylase-immunoreactive cells in caudal ventrolateral medulla were activated by both seizures and hypoxia (mean per cents, 79 and 67%, respectively). Since cell populations activated by seizures and hypoxia are indistinguishable, and a majority of tyrosine hydroxylase-reactive cells in caudal ventrolateral medulla are independently activated by each stimulus, it may be inferred that some impulses originating from seizures and chemoreceptor afferent pathways converge to a common set of neurons. These observations identify neurons in rat medulla oblongata which may mediate the impact of seizures on central processing of chemoreceptor afferent activity.

Animals↗

PubMed1981

Do arterial chemoreceptors play a role in the pathogenesis of hypertension?

Although the arterial chemoreflex exerts a powerful influence upon the cardiovascular system, this reflex has until now been a disregarded factor in hypertension research. By comparing the physiological effects of chemoreceptor excitation to disarrangements present during the early labile phase of hypertension in spontaneously hypertensive rats, we found remarkable similarities. A search through the literature as well as our experimental data fully confirm this association. Many factors, among them decreased blood flow through the glomic tissue, lead to chemoreceptor stimulation. The origins of the chemoreceptor arteries are located in areas very susceptible to atherosclerotic changes which can lead to ischemia of chemoreceptor tissue. We are led to hypothesize that arterial chemoreflex is a significant factor in the etiology of essential hypertension.

Animals↗

PubMed2005

Development of chemoreceptor responses in infants.

This paper is devoted to the field of chemoreception and its role in the control of breathing in infants. We use "chemoreception" to refer to the capacity to sense and process changes in P(O2) and P(CO2), and also to react to these changes by adjusting ventilation in order to maintain homeostasis. Functional chemoreceptors are not essential to commence or even to sustain breathing efforts immediately at or after birth; the intense brain activation, which occurs at birth, is sufficient. Over subsequent days to weeks, however, this "neurogenic" drive weakens and drive from the chemoreceptors becomes critical for generating and maintaining a normal breathing rhythm. Failure of the chemoreceptors to develop normally, consequently, becomes an important underlying cause of breathing dysfunction, particularly during sleep. The paper deals with the methods available to study chemoreception in newborn infants and provide an overview of the early postnatal changes and interactions, which influence breathing at rest and under stress. The latter may be described in terms of the threshold and strength as well as the delay/speed with which ventilation changes in response to chemical stimulation. We conclude with a survey of disorders associated with chemoreceptor deficits in infancy.

Animals↗

PubMed2006

Chemoreceptor and pulmonary stretch receptor interactions within amphibian respiratory control systems.

The hypercapnic drive to breathe in amphibians is generally greater than hypoxic ventilatory drive and a variety of interdependent control systems function to regulate both the hypoxic and hypercapnic ventilatory responses. During exposure to hypercapnic conditions, breathing increases in response to input from central chemoreceptors (sensitive to CSF pH/CO(2) levels) and peripheral chemoreceptors (sensitive to arterial blood O(2) and CO(2)). On the other hand, olfactory CO(2) receptors in the nasal epithelium inhibit breathing during exposure to acute hypercapnia. Further complexity arises from the CO(2)-sensitive nature of the pulmonary stretch receptors (PSR) which provide both tonic (stimulates lung inflation at low lung volumes; deflation at higher volumes) and phasic (generally excitatory) feedback. This review focuses on interactions between the various populations of chemoreceptors and interactions between chemoreceptors and PSR. Differences between various levels of experimental reduction (i.e., in vitro; in situ; in vivo) are highlighted as are the effects of chronic respiratory challenges on acute hypoxic and hypercapnic chemoreflexes.

Amphibians↗

PubMed2004

Maturation of peripheral arterial chemoreceptors in relation to neonatal apnoea.

Apnoea and periodic breathing are the hallmarks of breathing for the infant who is born prematurely. Sustained respiration is obtained through modulation of respiratory-related neurons with inputs from the periphery. The peripheral arterial chemoreceptors, uniquely and reflexly change ventilation in response to changes in oxygen tension. The chemoreflex in response to hypoxia is hyperventilation, bradycardia and vasoconstriction. The fast response time of the peripheral arterial chemoreceptors to changes in oxygen and carbon dioxide tension increases the risk of more periodicity in the breathing pattern. As a result of baseline hypoxaemia, peripheral arterial chemoreceptors contribute more to baseline breathing in premature than in term infants. While premature infants may have an augmented chemoreflex, infants who develop bronchopulmonary dysplasia have a blunted chemoreflex at term gestation. The development of chemosensitivity of the peripheral arterial chemoreceptors and environmental factors that might cause maldevelopment of chemosensitivity with continued maturation are reviewed in an attempt to help explain the physiology of apnoea of prematurity and the increased incidence of sudden infant death syndrome (SIDS) in infants born prematurely and those who are exposed to tobacco smoke.

Apnea↗

PubMed2002

A theoretical analysis of the carotid body chemoreceptor response to O2 and CO2 pressure changes.

A simple mathematical model of the carotid body chemoreceptor response is presented. The model assumes that the static chemoreceptor characteristic depends on oxygen saturation in the arterial blood and on CO2 arterial concentration. The values of O2 saturation and of CO2 concentration are computed, from pressure, using blood dissociation curves, which include both the Bohr and Haldane effects. Moreover, the O2-CO2 static responses interact via a multiplicative term followed by an upper saturation. The dynamic response includes a term depending on the time derivative of CO2 concentration and a low-pass filter, which accounts for the time required to reach the steady state level. With a suitable choice of its parameters, the model reproduces the carotid chemoreceptor response under a variety of combined O2 and CO2 stimuli, both in steady state conditions and in the transient period following acute CO2 or O2 pressure changes. In particular, simulations show that if two hypercapnic stimuli are given in rapid succession, the response to the second stimulus is weaker than the first. Moreover, during transient conditions the effect of CO2 pressure changes prevail over the effect of O2 changes, due to the intrinsic derivative component of the response to CO2. In conclusion, the model allows present knowledge about chemoreceptor activity to be summarized in a single theoretical framework. In perspective, it may be used as an afferent block within large-scale models of the overall cardio-respiratory control system.

Carbon Dioxide↗

PubMed1999

GABA(B) receptors in the nucleus tractus solitarii modulate the carotid chemoreceptor reflex in rats.

In urethane-chloralose anesthetized rats, the role of GABA(B) receptor in the commissural subnucleus of the nucleus tractus solitarii (commNTS) on the carotid chemoreceptor reflex was investigated. Microinjection of a GABA(B) agonist baclofen into the commNTS did not have any effects on arterial blood pressure (BP) or respiration (RP), while it attenuated the increases in BP and RP elicited by carotid chemoreceptor stimulation. These effects were blocked by microinjection of a GABA(B) antagonist 2-OH-saclofen into the same site. Prior microinjection of 2-OH-saclofen did not have any effects on the chemoreflex or on resting BP or RP, while the effects of baclofen on the chemoreflex were completely blocked. These results suggest that GABAB receptors are present in the carotid chemoreceptor reflex pathway in commNTS and modulate the chemoreceptor reflex.

Animals↗

PubMed2003

Atrial natriuretic peptide stimulates cat carotid body chemoreceptors in vivo.

It is known that atrial natriuretic peptide (ANP) is released from cardiac myocyte and other stores during hypoxia and is involved in pulmonary-cardiovascular reflexes and in natriuresis and diuresis. Since the carotid body initiates hypoxic chemoreflexes, we hypothesized that ANP could potentiate the hypoxic stimulation of the carotid body chemoreceptor in vivo. We studied the effect of close intra-arterial injection of ANP on carotid chemoreceptor activity in anesthetized male cats which were paralyzed and artificially ventilated. Graded doses of ANP (0-10 nmoles) were administered by intra-arterial injections and they produced an excitatory response. Single dose of ANP (6.5 nmoles) at four steady-state levels of arterial PO(2), at constant PCO(2), produced increases of chemoreceptor activity. This increase of chemoreceptor activity with ANP in the presence of CO(2)-HCO(3)(-) in vitro could make a difference from those without CO(2)-HCO(3)(-) in vivo.

Adaptation, Physiological↗

PubMed2002

CO2 dialysis in one chemoreceptor site, the RTN: stimulus intensity and sensitivity in the awake rat.

We stimulate single central chemoreceptor sites in the unanesthetized rat by focal microdialysis of artificial cerebrospinal fluid (aCSF) equilibrated with 25% CO(2). Here, in the retrotrapezoid nucleus (RTN) we measured the focal stimulus intensity with a pH electrode adjacent to the dialysis probe. During 25% CO(2) dialysis, RTN pH decreased by 0.069 (0.013, SEM) pH units (N=5), 44% of the change observed during 7% CO(2) breathing, -0.157 (0.019) pH units (N=4). During 7% CO(2) breathing, Pa(CO(2)) increased by 15 Torr (N=5). We calculate the deltaPa(CO(2)) that would produce a deltapH at the RTN approximately like that observed during 25% CO(2) dialysis as 44% of 15 Torr, or 6.6 Torr deltaPa(CO(2)). Using ventilatory response data from our lab, we estimate overall chemoreceptor sensitivity as 13% deltaVE/Torr deltaPa(CO(2)) and RTN sensitivity as 3% deltaVE/Torr deltaPa(CO(2)). The RTN provides 23% of the overall response. This may be an underestimate. During RTN stimulation Pa(CO(2)) decreases by 4.9 (0.7) Torr (N=5), which may inhibit other chemoreceptor sites. Multiple chemoreceptor sites may interact to provide high sensitivity in systemic hypercapnia and stability during heterogeneous stimulation and inhibition.

Animals↗

PubMed2004

Melatonin attenuates rat carotid chemoreceptor response to hypercapnic acidosis.

Respiratory activity is under circadian modulation and the physiological mechanisms may involve the pineal secretory product, melatonin, and the carotid chemoreceptor. We hypothesized that melatonin modulates the carotid chemoreceptor response to hypercapnic acidosis. To determine whether the effect of melatonin on the chemoreceptor response to hypercapnic acidosis is mediated by melatonin receptors in the chemosensitive cells, cytosolic calcium ([Ca2+]i) was measured by spectrofluorometry in fura-2-loaded glomus cells dissociated from rat carotid bodies. Melatonin (0.01-10 nm) per se did not change the [Ca2+]i levels of the glomus cells but it concentration-dependently attenuated the peak [Ca2+]i response to hypercapnic acidosis in the glomus cells. In addition, the [Ca2+]i response was attenuated by 2-iodomelatonin, an agonist of melatonin receptors. The melatonin-induced attenuation of the [Ca2+]i response to hypercapnic acidosis was abolished by pretreatment with an non-selective mt1/MT2 antagonist, luzindole, and by MT2 antagonists, 4-phenyl-2-propionamidotetraline or DH97. 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. Also, melatonin attenuated the carotid afferent response to hypercapnic acidosis in single- or pauci-fibers recorded from the sinus nerve in isolated carotid bodies superfused with bicarbonate-buffer saline. Results suggest that an activation of the melatonin receptors expressed in the glomus cells of the rat carotid body reduces the chemoreceptor response to hypercapnic acidosis. This modulation may play a physiological role in the influence of the circadian rhythms on the chemoreflex.

Acidosis, Respiratory↗

PubMed2004

Increased peripheral chemoreceptor activity may be critical in destabilizing breathing in neonates.

Periodic breathing and apnea are common in neonates, yet the physiological mechanisms involved are not clear. A low arterial PO2 might magnify peripheral chemoreceptor contribution to breathing, with its baseline variability inducing major changes in ventilation, leading to instability of the respiratory control system. We hypothesized that neonates: (1) would depend much more on the peripheral chemoreceptor contribution to breathing than adult subjects and (2) their baseline arterial PO2 would sit on the steep portion of the ventilation/arterial PO2 relationship on the adult nomogram, making breathing prone to oscillate. We analyzed data from previous polygraphic recordings in four groups of subjects: small preterm infants [SPI; postconceptional age (PCA) 33+/-2 weeks; n = 40], large preterm infants (LPI; PCA 36+/-2 weeks; n = 34), term infants (TI; PCA 42+/-1 week; n = 24), and adult subjects (AS; weight 63+/-2 kg; age 29+/-3 years, n = 16). Peripheral chemoreceptor activity was measured by: (1) the immediate decrease in ventilation and (2) apnea time during brief inhalation of 100% O2 (about 1 minute). We found that: (1) the immediate decrease in ventilation with 100% O2 was more pronounced in infants than in adult subjects (38+/-2 versus 6+/-5%), and in infants breathing periodically versus those breathing continuously; (2) the apnea time during 100% O2 was also significantly longer in periodic breathing infants; and (3) the TcPO2 was much lower in infants than in adult subjects (65+/-1 versus 93+/-1 Torr), and also lower in periodic versus continuously breathing infants. It was located significantly to the left of values for the adult subject, on the ventilation/arterial PO2 diagram. The data suggest that: (1) a substantial portion of baseline breathing activity early in life is maintained by increased peripheral chemoreceptor activity; and (2) neonates breathe irregularly with apneas due to the position of their arterial PO2 values on the ventilation/arterial PO2 diagram, in which a change in PO2 produces a more significant change in ventilation than that observed later in life.

Adult↗

PubMed2004

Attractant binding alters arrangement of chemoreceptor dimers within its cluster at a cell pole.

Many sensory systems involve multiple steps of signal amplification to produce a significant response. One such mechanism may be the clustering of transmembrane receptors. In bacterial chemotaxis, where a stoichiometric His-Asp phosphorelay from the kinase CheA to the response regulator CheY plays a central role, the chemoreceptors (methyl-accepting chemotaxis proteins) cluster together with CheA and the adaptor CheW, at a pole of a rod-shaped cell. This clustering led to a proposal that signal amplification occurs through an interaction between chemoreceptor homodimers. Here, by using in vivo disulfide crosslinking assays, we examined an interdimer interaction of the aspartate chemoreceptor (Tar). Two cysteine residues were introduced into Tar: one at the subunit interface and the other at the external surface of the dimer. Crosslinked dimers and higher oligomers (especially a deduced hexamer) were detected and their abundance depended on CheA and CheW. The ligand aspartate significantly reduced the amounts of higher oligomers but did not affect the polar localization of Tar-GFP. Thus, the binding of aspartate alters the rate of collisions between Tar dimers in assembled signaling complexes, most likely due to a change in the relative positions or trajectories of the dimers. These collisions could occur within a trimer-ofdimers predicted by crystallography, or between such trimers. These results are consistent with the proposal that the interaction of chemoreceptor dimers is involved in signal transduction.

Aspartic Acid↗

PubMed1995

Functional and developmental studies of the peripheral arterial chemoreceptors in rat: effects of nicotine and possible relation to sudden infant death syndrome.

The drive on respiration mediated by the peripheral arterial chemoreceptors was assessed by the hyperoxic test in 3-day-old rat pups. They accounted for 22.5 +/- 8.8% during control conditions, but only for 6.9 +/- 10.0% after nicotine exposure, an effect counteracted by blockade of peripheral dopamine type 2 receptors (DA2Rs). Furthermore, nicotine reduced dopamine (DA) content and increased the expression of tyrosine hydroxylase (TH) in the carotid bodies, further suggesting that DA mediates the acute effect of nicotine on arterial chemoreceptor function. During postnatal development TH and DA2R mRNA levels in the carotid bodies decreased. Thus, nicotine from smoking may also interfere with the postnatal resetting of the oxygen sensitivity of the peripheral arterial chemoreceptors by increasing carotid body TH mRNA, as well as DA release in this period. Collectively these effects of nicotine on the peripheral arterial chemoreceptors may increase the vulnerability to hypoxic episodes and attenuate the protective chemoreflex response. These mechanisms may underlie the well-known relation between maternal smoking and sudden infant death syndrome.

Animals↗

PubMed1982

Halothane depresses the response of carotid body chemoreceptors to hypoxia and hypercapnia in the cat.

Halothane is known to inhibit the ventilatory responses to hypoxia and hypercapnia. In order to determine whether this inhibition was mediated by peripheral chemoreceptors, the authors measured the effect of halothane on the response of carotid body chemoreceptors to these stimuli. Cats were decerebrated under brief halothane anesthesia, paralyzed, and ventilated. Chemoreceptor activity was recorded from single- or few-fiber preparations of carotid sinus nerve, and the inspiratory drive was recorded from the whole phrenic nerve. Steady-state responses were measured at three levels of CO2 tension (19-92 mmHg) during hyperoxia, and at four levels of O2 tension (35-450 mmHg) at a fixed PaCO2. Both responses were measured before, during, and after 0.5-1.0 per cent halothane was inspired. The halothane inhalation was maintained for at least 30 min before the responses were obtained. Halothane reduced the slope of chemoreceptor response to hypercapnia to about 48 per cent of the control slope. The response to hypoxia was reduced to about 58 pr cent of the control response. The increase in firing after intravenous nicotine (100 micrograms), summed for 20 s, was reduced to 25 per cent of the prehalothane control values; that after NaCN (25 micrograms) was reduced to 17 per cent of the control value. The effect of halothane was prompt (half complete in 1-2 min) and reversible. This finding explains some of the inhibition of the ventilatory responses to hypoxia and hypercapnia caused by halothane.

Animals↗

PubMed2005

Diagnostic cross-linking of paired cysteine pairs demonstrates homologous structures for two chemoreceptor domains with low sequence identity.

Hundreds of bacterial chemoreceptors from many species have periplasmic, ligand-recognition domains of approximately the same size, but little or no sequence identity. The only structure determined is for the periplasmic domain of chemoreceptor Tar from Salmonella and Escherichia coli. Do sequence-divergent but similarly sized chemoreceptor periplasmic domains have related structures? We addressed this issue for the periplasmic domain of chemoreceptor Trg(E) from E. coli, which has a low level of sequence similarity to Tar, by combining homology modeling and diagnostic cross-linking between pairs of introduced cysteines. A homology model of the Trg(E) domain was created using the homodimeric, four-helix bundle structure of the Tar(S) domain from Salmonella. In this model, we chose four pairs of positions at which introduced cysteines would be sufficiently close to form disulfides across each of four different helical interfaces. For each pair we chose a second pair, in which one cysteine of the original pair was shifted by one position around the helix and thus would be less favorably placed for disulfide formation. We created genes coding for proteins containing four such pairs of cysteine pairs and investigated disulfide formation in vivo as well as functional consequences of the substitutions and disulfides between neighboring helices. Results of the experimental tests provided strong support for the accuracy of the model, indicating that the Trg(E) periplasmic domain is very similar to the Tar(S) domain. Diagnostic cross-linking of paired pairs of introduced cysteines could be applied generally as a stringent test of homology models.

Amino Acid Sequence↗