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At least 487 records · Page 27Linked to original sources
PubMed1998

Angiotensin AT1 receptor-mediated excitation of rat carotid body chemoreceptor afferent activity.

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. Displacement studies demonstrated that the receptors were of the AT1 subtype. 2. The binding pattern indicated that the AT1 receptors occurred over clumps of glomus cells, the principal chemoreceptor cell of the carotid body. Selective lesions of the sympathetic or afferent innervation of the carotid body had little effect on the density of receptor binding, demonstrating that the majority of AT1 receptors were intrinsic to the glomus cells. 3. To determine the direct effect of angiotensin II on chemoreceptor function, without the confounding effects of the vasoconstrictor action of angiotensin II, carotid sinus nerve activity was recorded from the isolated carotid body in vitro. The carotid body was superfused with Tyrode solution saturated with carbogen (95 % O2, 5 % CO2), maintained at 36 C, and multi-unit nerve activity recorded with a suction electrode. 4. Angiotensin II elicited a dose-dependent excitation of carotid sinus nerve activity (maximum increase of 36 +/- 11 % with 10 nM angiotensin II) with a threshold concentration of 1 nM. The response was blocked by the addition of an AT1 receptor antagonist, losartan (1 microM), but not by the addition of an AT2 receptor antagonist, PD123319 (1 microM). 5. In approximately 50 % of experiments the excitation was preceded by an inhibition of activity (maximum decrease of 24 +/- 8 % with 10 nM angiotensin II). This inhibitory response was markedly attenuated by losartan but not affected by PD123319. 6. These observations demonstrate that angiotensin II, acting through AT1 receptors located on glomus cells in the carotid body, can directly alter carotid chemoreceptor afferent activity. This provides a means whereby humoral information about fluid and electrolyte homeostasis might influence control of cardiorespiratory function.

1-Sarcosine-8-Isoleucine Angiotensin II↗
PubMed1983

On the specificity and type of receptor involved in carotid body chemoreceptor activation by adenosine in the cat.

Experiments were performed on cats anaesthetized with pentobarbitone in which carotid chemoreceptor activity was recorded from the peripheral end of a sectioned carotid sinus nerve. Intracarotid injections of adenosine 5'-triphosphate (ATP) (1-100 micrograms i.c.) caused a dose-related increase in chemosensory discharge which was delayed in onset. The adenosine uptake inhibitor dipyridamole potentiated the chemoexcitatory effects of injected adenosine and ATP. The stable ATP analogue alpha-beta-methylene ATP (10-100 micrograms i.c.) depressed chemoreceptor discharge, which suggests the presence of a P2-purinoceptor in the carotid body, and provides evidence that the chemoexcitatory effect of ATP results from its hydrolysis to adenosine 5'-phosphate (AMP)/adenosine. Adenine, inosine, guanosine, cytidine and uridine had no appreciable effect on chemoreceptor discharge. The adenosine R-site agonists 2'-chloroadenosine and N6-methyladenosine had chemoexcitatory effects which were similar to those of adenosine, whereas the P-site agonist 2'-deoxyadenosine had no appreciable effect on discharge. We conclude that the adenosine receptor in the cat carotid body has some of the characteristics of an R-site receptor according to the classification of Londos & Wolff (1977).

Adenosine↗
PubMed1968

Activity of aortic chemoreceptors during electrical stimulation of the stellate ganglion in the cat.

1. In anaesthetized cats, action potentials from aortic chemoreceptors were recorded during electrical stimulation of preganglionic sympathetic fibres to the decentralized right stellate ganglion. The rate of discharge in afferents in the ipsilateral but not in the contralateral aortic nerve increased when stimulus frequency was 4/sec or higher.2. The post-ganglionic fibres in the stimulated pathway originate in the right stellate ganglion. They leave the ganglion in the caudal limb of the ansa subclavia, and the results suggest that the ipsilateral aortic nerve and its branches distribute sympathetic fibres as well as afferents to aortic bodies.3. In contrast, the rate of discharge of chemoreceptor fibres in the contralateral aortic nerve fell as blood pressure increased during sympathetic stimulation. Sympathetic pathways to the aortic bodies can maintain or increase chemoreceptor discharge during hypertension elicited by sympathetic activation.

Journal Article↗
PubMed1978

Effect of cholinergic antagonists on sympathetic ganglionic transmission of vasomotor reflexes from the carotid baroreceptors and chemoreceptors of the dog.

1. In anaesthetized dogs the reflex vascular resistance changes in a perfused hind limb were studied following carotid baroreceptor or chemoreceptor stimulation. 2. The observed rises in resistance were sympathetically mediated and thus provided a means of studying the action of the cholinergic antagonists on the sympathetic ganglion transmission. 3. The reflex response to carotid baroreceptor stimulation produced by lowering the pressure in the carotid sinuses was abolished by hexamethonium bromide but not reduced by hyoscine methyl bromide. 4. The reflex response to carotid body chemoreceptor stimulation, by hypoxia, was not altered by hexamethonium bromide but was greatly reduced by the hyoscine methyl bromide. No reflex response was seen when both antagonists were present. 5. These results indicate that sympathetic ganglion synaptic transmission during the baroreceptor reflex is mediated by nicotinic receptor activation. The transmission evoked by chemoreceptor stimulation involves muscarinic receptors with a subsidiary nicotinic pathway. High doses of an antagonist were necessary to block the muscarinic component of transmission and this is discussed in relation to previous work. 6. No non-cholinergic transmission of the reflex responses was observed.

Animals↗
PubMed1979

Left ventricular inotropic responses to stimulation of carotid body chemoreceptors in anaesthetized dogs.

1. Dogs were anaesthetized with chloralose and artificially ventilated. The regions of both carotid bifurcations were vascularly isolated and perfused at constant pressure with arterial blood or with venous or hypoxic blood. 2. Inotropic responses were assessed by measuring the maximum rate of change of left ventricular pressure (dP/dtmax) with aortic pressure and heart rate held constant. 3. Stimulation of the chemoreceptors with venous blood from the inferior vena cava resulted in a decrease in dP/dtmax from 510 +/- 27 kPa.s-1 to 418 +/- 21 kPa.s-1 (mean +/- S.E.): a change of 17.9 +/- 1.0% 4. In experiments in which the oxygen tension of the blood perfusing the carotid chemoreceptors was decreased in steps between 10 and 3 kPa, by use of an oxygenator, graded responses of dP/dtmax were obtained at each step. 5. The inotropic responses to chemoreceptor stimulation were abolished by raising carotid pressure. 6. The inotropic responses were abolished either by crushing both carotid bodies or both ansae subclaviae, indicating that the reflex originates from the carotid bodies and that the efferent pathway is in the cardiac sympathetic nerves.

Animals↗
PubMed1977

Carotid body chemoreceptor reflexes and their interactions in the seal.

In the anesthetized spontaneously breathing harbor seal Phoca vitulina stimulation of the carotid body chemoreceptors by intracarotid injections of sodium cyanide or by hypoxic hypercapnic blood causes an increase in tidal volume, respiratory frequency, and respiratory minute volume. The heart rate invariably decreased. Experimental dives caused apnea and bradycardia. When the carotid bodies are stimulated within 10 s of the commencement of a dive, the chemoreceptor-respiratory response is abolished, but the chemoreceptor-cardioinhibitory response is considerably enhanced. Electrical stimulation of the central cut end of a superior laryngeal nerve also causes apnea and bradycardia; stimulation of the carotid body now fails to produce a respiratory response but the cardioinhibitory effect is enhanced. These results indicate that the carotid bodies cause reflexly hyperventilation and bradycardia, and that these responses are considerably modified by other inputs to the central nervous system.

Animals↗
PubMed1976

Analysis of inhibitory effect of dopamine on carotid body chemoreceptors in cats.

The inhibitory effect of dopamine on carotid body chemoreceptors was studied in anesthetized cats to determine whether it was dependent on changes in blood flow in the vicinity of the receptors. The blood supply to the carotid body was isolated, and flow was controlled with a perfusion pump. Single- or few-fiber recordings were made from the peripheral end of the cut carotid sinus nerve in seven cats. The rate of discharge of 68 chemoreceptor strands increased when flow through the carotid body was stopped. This response was reduced or abolished by dopamine in animals ventilated with either room air (15 strands) or a gas mixture of 95% O2 and 5% CO2 (53 strands). These results suggest that dopamine exerts its inhibitory effect primarily through a direct action on the chemoreceptors rather than by a vasomotor effect in the carotid body.

Animals↗
PubMed1982

Stimulation of carotid chemoreceptors and ventilation by doxapram in the cat.

Small doses of doxapram (less than 0.5 mg . kg-1 iv) were used to study its effect on carotid chemoreceptor activity and ventilation in cats anesthesized with alpha-chloralose. The effects were studied at several levels of partial pressures of O2 and CO2 in arterial blood (PaO2 and PaCO2). It was found that doxapram stimulated discharge rate of the carotid chemoreceptor afferents by the same magnitude at all levels of PaO2 and PaCO2 studied. However, the ventilatory effect of doxapram was more than additive to the concomitant stimulation by hypoxia or hypercapnia. This ventilatory effect was eliminated by sectioning the carotid sinus and aortic nerves. These results led to the conclusion that the ventilatory stimulus interaction due to doxapram is dependent on the excitatory input from the peripheral chemoreceptors.

Anesthesia↗
PubMed1987

Role of substance P in hypercapnic excitation of carotid chemoreceptors.

Experiments were performed on 17 anesthetized, paralyzed, and artificially ventilated cats to evaluate the importance of substance P-like peptide (SP) on the carotid body responses to CO2. Single or paucifiber carotid chemoreceptor activity was recorded from the peripheral end of the cut carotid sinus nerve. In eight of the cats the influence of SP on hyperoxic hypercapnic responses was studied. While the animals breathed 100% O2, intracarotid infusion of SP (1 microgram.kg-1.min-1, 3 min) increased chemoreceptor activity by +4.8 +/- 0.3 impulses/s. After SP infusion, inhalation of CO2 in O2 caused a rapid increase in activity that reached a peak and then adapted to a lower level, whereas similar levels of CO2 before SP caused only a gradual increase in carotid body discharge rate without any overshoot in response. Furthermore SP significantly increased the magnitude and slope of the CO2 response. In the other nine cats the effect of intracarotid infusion of an SP antagonist, [D-Pro2,D-Trp7,9] SP (10-15 micrograms.kg-1.min-1), on carotid body responses to 1) hyperoxic hypercapnia (7% CO2-93% O2), 2) isocapnic hypoxia (11% O2-89% N2), and 3) hypoxic hypercapnia (11% O2-7% CO2-82% N2) was examined. SP antagonist had no effect on carotid body response to hyperoxic hypercapnia but significantly attenuated the chemoreceptor excitation caused by isocapnic hypoxia and hypoxic hypercapnia. These results suggest that 1) SP may play an important role in carotid body responses to hypoxia but not to CO2, and 2) the mechanisms of stimulation of the carotid body by hypercapnia and by hypoxia differ.

Animals↗
PubMed1989

Stimulus interaction between CO2 and almitrine in the cat carotid chemoreceptors.

The hypothesis that augmentation of the carotid chemoreceptor response to hypoxia by almitrine is due in part to an increased response to CO2 was tested by using single or few fiber preparation of carotid body chemosensory fibers in 12 cats anesthetized with alpha-chloralose. To differentiate between the plausible mechanisms of effects, we also tested the responsiveness of the afferents to cyanide and nicotine before and after almitrine. After a saturation dose of almitrine (1 mg.kg-1 followed by 0.5 mg.kg-1.h-1) the chemosensory responses to CO2 strikingly increased even during hyperoxia: the afferents showing an increased transient peak activity at the onset of hypercapnia, an augmented steady-state response to CO2 stimulus, and a decreased arterial PCO2 stimulus threshold. Thus, the effect of almitrine on carotid chemoreceptor response to hypoxia could be explained, at least in part, by its multiplicative stimulus interaction with CO2. After almitrine, the chemoreceptor response to cyanide, which is dependent on arterial PO2, was not particularly augmented relative to those of nicotine. Accordingly, the O2-sensing mechanism does not appear to be the primary site of almitrine effect. The results also indicate that the site of CO2 chemoreception resides downstream from those of hypoxia.

Almitrine↗
PubMed1989

Ventilatory control during exercise with peripheral chemoreceptor stimulation: hypoxia vs. domperidone.

Hypoxia potentiates the ventilatory response to exercise, eliciting a greater decrease in arterial PCO2 (PaCO2) from rest to exercise than in normoxia. The mechanism of this hypoxia-exercise interaction requires intact carotid chemoreceptors. To determine whether carotid chemoreceptor stimulation alone is sufficient to elicit the mechanism without whole body hypoxia, ventilatory responses to treadmill exercise were compared in goats during hyperoxic control conditions, moderate hypoxia (PaO2 = 38-44 Torr), and peripheral chemoreceptor stimulation with the peripheral dopamine D2-receptor antagonist, domperidone (Dom; 0.5 mg/kg iv). Measurements with Dom were made in both hyperoxia (Dom) and hypoxia (Dom/hypoxia). Finally, ventilatory responses to inspired CO2 at rest were compared in each experimental condition because enhanced CO2 chemoreception might be expected to blunt the PaCO2 decrease during exercise. At rest, PaCO2 decreased from control with Dom (-5.0 +/- 0.9 Torr), hypoxia (-4.1 +/- 0.5 Torr), and Dom/hypoxia (-11.1 +/- 1.2 Torr). The PaCO2 decrease from rest to exercise was not significantly different between control (-1.7 +/- 0.6 Torr) and Dom (-1.4 +/- 0.8 Torr) but was significantly greater in hypoxia (-4.3 +/- 0.7 Torr) and Dom/hypoxia (-3.5 +/- 0.9 Torr). The slope of the ventilation vs. CO2 production relationship in exercise increased with Dom (16%), hypoxia (18%), and Dom/hypoxia (68%). Ventilatory responses to inspired CO2 at rest increased from control to Dom (236%) and Dom/hypoxia (295%) and increased in four of five goats in hypoxia (mean 317%).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Effects of domperidone on neonatal and adult carotid chemoreceptors in the cat.

It has been postulated that the weak carotid chemoreceptor responses of neonatal mammals may be due to inhibition produced by high levels of endogenous dopamine release or exaggerated sensitivity to dopaminergic inhibition. This was studied by measuring the effect of domperidone, a selective dopamine D2-receptor antagonist, on the carotid chemoreceptor response to O2 and CO2 in anesthetized neonatal and adult cats. The animals were exposed to four levels of isocapnic O2 (arterial PO2 of approximately 35-45, 55-65, 80-90, > 300 Torr) and four levels of isoxic CO2 (end-tidal PCO2 of approximately 21, 40, 58, and 78 Torr) before and after D2-receptor blockade. Whole nerve activity was recorded from the carotid sinus nerve (CSN). Both neonatal and adult cats increase CSN activity during hypoxia and hypercapnia (P < 0.001). Domperidone caused an increase in CSN activity at all O2 levels in adults (P < 0.01) but only during hypoxia in neonates (P < 0.001). Domperidone caused an increase in CSN activity during normo- and hypercapnia in adults but only during hypercapnia in neonates (P < 0.001). Domperidone approximately doubled an index of hypoxic sensitivity in the normoxia-hypoxia range (100 to 40 Torr) in the neonatal group but had little effect on sensitivity to hypoxia in adults. We conclude that the inhibitory role of endogenous dopamine in the carotid chemoreceptors changes with postnatal development.

Animals↗
PubMed1979

Effects of chemoreceptor and baroreceptor stimulation on the discharge of hypothalamic supraoptic neurones in rats.

Experiments have been performed to examine the effects of activating the carotid body chemoreceptors and the arterial baroreceptors on the discharge of neurones within the hypothalamic supraoptic nucleus of the rat. Chemoreceptors were activated by intracarotid injection of 0.9% NaCl solution equilibrated with 100% CO2. The baroreceptors of the carotid sinus and aortic arch were activated by raising the blood pressure with an intravenous injection of phenylephrine. Chemoreceptor stimulation activated and baroreceptor stimulation inhibited the discharge of all the phasically discharging neurones tested. Neither stimulus had any consistent effect on non-phasically discharging neurones, although slight inhibition occasionally occurred. Anaesthesia of the carotid bifurcation abolished the effects of cardiovascular stimulation on the supraoptic neurones. Responses resumed when the anaesthesia wore off. However, the anaesthesia also seemed to alter the phasic pattern of discharge. The results are discussed with reference to the influence of the cardiovascular receptors upon the neurones in the supraoptic nucleus, and with reference to possible roles for the cardiovascular reflexes in control of vasopressin secretion.

Action Potentials↗
PubMed1976

[Effect of thrombin on chemoreceptors of the frog carotid labyrinth].

The frog's electrical activity of the carotid body chemoreceptors reacting to thrombin was studied. The chemoreceptor response was estimated by means of afferent impulsation in the n. glossopharingeus. The afferent impulsation frequency increases to a certain extent in proportion to the irritant concentration; too high a thrombin concentration is able to suppress the chemoreceptor activity. The direct dependence between the receptor response and the effector reaction diminishing the blood coagulation, was established. The receptors adapt slowly, their discharge is of an irregular character.

Animals↗
PubMed1990

Role of the carotid chemoreceptors in the respiratory response of newborn lambs to alternate pairs of breaths of air and a hypoxic gas.

We measured the reflex respiratory response to a 2-breath alternation in fractional inspired oxygen in two groups of lambs. Test runs where F(I),O2 was made to alternate (between 0.21 and 0.14) were compared with control runs in which it was held at 0.21. Within 36 h of birth we cut the carotid sinus nerves bilaterally in one group of lambs (n = 5) whilst in a second group (n = 5) sham operations were carried out. The alternating responses in seven respiratory variables were compared between test and control runs in each group of lambs at postnatal days 5-6 and again at postnatal days 10-11. In sham-operated lambs at days 5-6 there was a significant response in most respiratory variables during test runs and by days 10-11 the response was increased, primarily as a consequence of an increase in the tidal volume component of the response, indicating a postnatal maturation of the responses. The time-scale of this maturation is appropriate to that of peripheral chemoreceptor resetting. There was no significant response to the test in the denervated lambs at 5-6 days but by days 10-11 a small response was measured in some variables. Our results therefore indicate that the reflex respiratory response to alternations in FI,O2 is primarily mediated by the carotid chemoreceptors. The development of a response mediated by the aortic chemoreceptors may account for the small alternating response in the denervated lambs at days 10-11.

Animals↗
PubMed1989

Fentanyl inhibits the canine carotid chemoreceptor reflex.

To investigate the impact of fentanyl on the carotid chemoreceptor reflex, nine mongrel dogs were permanently monitored with electromagnetic flow transducers around the right common iliac artery and with heparin-filled catheters in the descending aorta and in one of the main carotid arteries with the tip just proximal to the carotid sinus. Carotid chemoreceptor activation (CCRA) produced by consecutive injections of nicotine (0.2-0.4 micrograms/kg) through the carotid catheter elicited bradycardia, expressed as an increase in cardiac cycle length by 140% +/- 18%, and a 252% +/- 16% increase in mean iliac arterial vascular resistance. These responses were markedly attenuated by fentanyl in a dose-dependent fashion: cardiac cycle length increased only by 50% +/- 7% (P less than 0.01) with 4 micrograms/kg and by 19% +/- 6% (P less than 0.01) with 8 micrograms/kg of intravenous fentanyl. These changes were paralleled by significantly (P less than 0.01) lesser increases in mean iliac arterial resistance (122% +/- 9% and 50% +/- 5%). It is concluded that fentanyl impairs the integrity of the carotid chemoreceptor reflex.

Animals↗
PubMed1982

Effects of vagal stimulation and carotid body chemoreceptor stimulating agents on phrenic nerve activity in vagotomized rabbits.

Effects of vagal stimulation and carotid body chemoreceptor stimulating agents on phrenic nerve activity were studied in vagotomized rabbits. The decreases of TI and IPA were proportional to the increase of stimulus frequency and these inhibitory effects were rapidly reversed after vagal stimulation was discontinued. The continuous vagal stimulation at low frequency resulted in a marked potentiation of TI accompanied by a decrease of IPA. The prolongation of TI caused by subthreshold vagal stimulation which failed to terminate the inspiration may probably be due to the inhibition of the PC phasic activity. An intracarotid injection of NaCN led to a decrease of TI and it showed a marked potentiation of IPA. DA and 5-HT showed apneustic respiratory patterns in phrenic responses associated with a slight increase of IPA. Therefore, it may be suggested that the afferent inputs from carotid body chemoreceptor by DA and 5-HT are projected to the I beta neurons in the NTS whereas the input from NaCN-stimulated carotid body chemoreceptor is projected into the I alpha neurons.

Animals↗
PubMed1997

Immunocytochemical localization on O2-sensing protein (NADPH oxidase) in chemoreceptor cells.

A potential candidate for an oxygen-sensing protein in chemoreceptor cells is a heme-linked multicomponent NADPH oxidase, originally described in neutrophils. The postulated function for the oxidase in chemoreceptor cells is to signal changes in oxygen levels (either in the blood or in the airway lumen) via changes in oxygen metabolite production. An alteration in either superoxide (or dismuted hydrogen peroxide) production may affect the gating properties of the O2-sensitive K+ channels. We have previously reported immunohistochemical localization of gp91 glycoprotein component of the oxidase to the plasma membrane of pulmonary neuroepithelial body (NEB) cells. In this study we have investigated the immunocytochemical localization of the other polypeptide components of the oxidase in NEB cells and in the glomus cells of the carotid body. Cultures of dissociated fetal rabbit NEB cells and newborn rat glomus cells were immunostained with specific antibodies recognizing the various polypeptide subunits of the oxidase using indirect immunofluorescence methods. Immunostaining with the anti-oxidase antibodies reveal strong positive reaction in both NEB and glomus cell clusters while other cells were unstained. The positive reaction product was localized to the plasma membrane and/or cytoplasm and no nuclear staining was observed. Live cell labelling studies with anti-p22 antibody showed positive immunofluorescence on the surface of NEB cells, suggesting that this component of the oxidase is also associated with the plasma membrane. In glomus cells, similar strongly positive immunofluorescence signal was observed for p22 and gp91 in paraformaldehyde-fixed cultures, regardless whether they were permeabilized or not. Taken together, our findings of cell surface localization of gp91 and p22 components of the oxidase in chemoreceptive cells suggests that the heme-linked cytochrome b558 component is associated with the plasma membrane. This association allows for direct interaction with the O2-sensitive K+ channel thus forming the molecular complex of membrane bound O2 sensor.

Animals↗