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PubMed1987

Excitation of carotid body chemoreceptors by neuropeptide-Y.

Neuropeptide-Y (NPY) is a peptide co-localised with noradrenaline in many sympathetic nerves. Recently, it has been found in postganglionic sympathetic nerves running to blood vessels in the carotid body. When NPY is administered to cats by infusion into the arterial blood close to the carotid bodies, breathing is stimulated. This effect is abolished when the carotid sinus nerves are cut. Similar intra-carotid infusions of NPY can be demonstrated to increase the frequency of firing of chemoreceptor afferent nerves. However, NPY introduced into the blood vessels of the carotid body immediately prior to halting its blood flow does not modify the development of chemoreceptor discharge in response to developing asphyxia. The findings are consistent with NPY causing excitation of chemoreceptors by causing local vasoconstriction and stagnant asphyxia.

Animals↗

PubMed1988

The effect of almitrine bismesylate on the steady-state responses of arterial chemoreceptors to CO2 and O2 in the cat.

The interaction between almitrine bismesylate, a pharmacological stimulant of peripheral chemoreceptors, and varying levels of oxygen (PO2 50-600 Torr) and carbon dioxide (PCO2 10-65 Torr) on steady state carotid chemoreceptor discharge was investigated in pentobarbitone-anaesthetised cats. Almitrine was given as constant intravenous (50 micrograms/kg per min for 4 min) and intracarotid infusions (4-16 micrograms/kg per min) at different levels of alveolar PO2 and PCO2. Almitrine always excited discharge. The intracarotid infusions at the lower infusion rate (4-8 micrograms/kg per min) and the i.v. infusions increased the slope of the isoxic response to CO2. This effect could be reversed by raising PO2 to high levels. Higher infusion rates of almitrine (16 micrograms/kg per min) displaced the CO2 response curve upwards but did not increase its slope above that obtained in control conditions at end-tidal PO2 of 50 Torr. However, as these higher infusion rates caused levels of discharge greater than those achieved during control conditions, their effects on control CO2 sensitivity could not be ascertained. Our results suggest that almitrine excites carotid body chemoreceptors by a mechanism similar to that of hypoxia and not like that of carbon dioxide.

Almitrine↗

PubMed1988

The effect of hypoxia on the response of the carotid body chemoreceptor to potassium in the anaesthetized cat.

The effect of hypoxia on the response of the carotid chemoreceptor to potassium has been investigated in anaesthetized cats. After an initial period of ventilation on air, FIO2 was reduced to 0.1-0.13 to give a mean PaO2 of 44 mm Hg. KCl was infused intravenously to raise arterial K+ to approximately 6 mM and hold it at that level. For 8 experiments in 7 cats, mean chemoreceptor discharge increased from 1.9 impulses.sec-1 on air, to 7.3 impulses.sec-1 during hypoxia to a peak of 12.2 impulses.sec-1 after the first 0.25 min of the potassium infusion. The initial speed of response and pattern of adaptation were similar to those seen in normoxic cats, but the combined effects of hypoxia and hyperkalaemia on carotid chemoreceptor discharge were greater than the sum of the individual effects.

Animals↗

PubMed1989

Central-peripheral chemoreceptor ventilatory interaction in awake goats.

This study was designed to characterize the ventilatory interaction between central and carotid body (CB) chemoreceptor stimulation in awake goats undergoing selective CB perfusion. This model allowed us to expose central and CB chemoreceptors to separate blood gas conditions in an animal that is conscious and not systemically hypoxic. Systemic CO2 ventilatory response curves, performed by progressively increasing FICO2 in systemic hyperoxia, were completed in 7 goats during CB perfusion with hypercapnic-hypoxic blood and normocapnic-normoxic blood, and in 3 goats without CB perfusion. The slopes of the curves done with perfusion were not significantly different (P greater than 0.05) in CB hypercapnic hypoxia and CB normocapnic normoxia for VE, VT, f and VT/TI, and the coefficients of variation of slopes generated with and without perfusion were similar. Our data indicate there is addition of central and CB chemoreceptor input in respiratory control, and we conclude that the previously demonstrated stimulus interaction at the CB is the primary source of the hyperadditive hypercapnic-hypoxic ventilatory interaction in an animal unaffected by anesthetics or brain hypoxia.

Animals↗

PubMed1990

Carotid chemoreceptor response to increases in CO2 output.

The effect on carotid chemoreceptor activity of alterations in PaCO2 oscillations produced by venous CO2 loading via the small intestines was studied in anaesthetised cats, which were paralysed and ventilated at constant frequency. Changes in PaCO2 oscillations were assessed from continuously recorded oscillations of arterial pH. Chemoreceptor activity was averaged over 20-50 pH cycles to determine the amplitude (csnd ampl) and mean level (csnd mean) of the respiratory fluctuation in discharge frequency during control and CO2 loaded periods. Two groups of 5 cats were studied. In both groups, the amplitude of the PaCO2 oscillations increased by an overall average of 74.5% (standard error, SE = 9.2) with minimal change in mean PaCO2 (average increase 0.7 mm Hg), in response to an increase in VCO2 of 77.5% (SE = 7.4). When isoxia was maintained (Group 1) csnd ampl increased by 51.3% (SE = 11.1) and csnd mean by 17.3% (SE = 7.8). In Group 2, PaO2 rose by 16.7 mm Hg (SE = 1.5) during CO2 loading and both csnd ampl and csnd mean decreased by 7.4% (SE = 9.3) and 2.3% (SE = 13.3) respectively. The results demonstrate a sensitivity of chemoreceptors to changes in VCO2 which is influenced by small changes in PaO2.

Animals↗

PubMed1992

Chemoreceptor control of the airways.

The peripheral chemoreceptors act reflexly not only on respiration, but also on many motor systems in the respiratory tract. They cause a reflex bronchoconstriction, although this may be modified or even reversed by secondary dilator reflexes such as that from pulmonary stretch receptors. They promote a reflex secretion of mucus from submucosal glands in the trachea, and possibly other parts of the airways. They cause systemic reflex vasoconstriction both in nose (with reduction in airflow resistance) and trachea, and probably in the bronchi. There is also a reflex pulmonary vasoconstriction, although the strength of this has not been determined. The larynx dilates during peripheral chemoreceptor stimulation, as does the oropharynx. All these changes affect airway calibre, most components increasing it but some having the opposite effect. In turn these airway responses will affect lung ventilation and blood-gas tensions. The whole respiratory tract seems to be an important target organ for reflexes from the peripheral chemoreceptors.

Animals↗

PubMedDate not supplied

Functional characteristics of arterial chemoreceptors in an amphibian (Bufo marinus).

In order to further describe the functional characteristics of arterial chemoreceptors of anuran amphibians, multi-unit chemoreceptor discharge frequency (MCDF) was recorded from the carotid (N = 23) or aortic nerve (N = 2) of pithed, unidirectionally ventilated toads (Bufo marinus). MCDF increased with decreasing PaO2: typically, the threshold PaO2 lay between 40 and 60 mmHg. The MCDF-PaO2 relationship was right-shifted along the PaO2 axis by increasing PaCO2 (N = 5). In three toads, the MCDF-PaO2 relationship was unaffected when CaO2 was reduced 35-89% by hemorrhage. MCDF was also unaffected by occlusion of the outflow from the heart, though it increased upon release of the occlusion. MCDF was stimulated by epinephrine, and inhibited by dopamine. Our results demonstrate that the MCDF responds to the range of PaO2 and PaCO2 values encountered in vivo, suggesting that arterial chemoreceptors may participate in ventilatory control in toads. The receptors do not respond to the rate of oxygen delivery per se, and may be influenced by catecholamines known to exist in the carotid labyrinth.

Animals↗

PubMed1994

Central chemoreceptor stimulus in the terrestrial, pulmonate snail, Helix aspersa.

We studied the effect of hypercapnic and fixed acid central chemoreceptor stimulation on the pneumostome in the pulmonate snail, Helix aspersa. We found that focal stimulation of the central chemoreceptor area of the pulmonate snail brain with hypercapnic solutions more effectively increased the pneumostomal area than did fixed acid stimulation at the same extracellular pH. Disrupting intracellular pH regulation by inhibiting Cl- transport, either pharmacologically (DIDS) or by ion substitution (Cl(-)-free perfusate), enhanced pneumostomal responses to CO2. While maintaining a constant perfusate pH, addition of NH4Cl to the perfusate resulted in pneumostomal closure; whereas removal of NH4Cl from the bath resulted in pneumostomal opening. In conclusion, the ventilatory response to CO2 in H. aspersa does not require Cl- transport or conductance. Furthermore, changing pHi alone is an adequate stimulus for the central chemoreceptors in the snail.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗

PubMed1995

Cardio-ventilatory control in rainbow trout: I. Pharmacology of branchial, oxygen-sensitive chemoreceptors.

The effects of various neurochemicals on O2-sensitive chemoreceptor afferent discharge in the glossopharyngeal nerve (cranial nerve IX) were examined in an isolated, perfused first gill arch preparation from rainbow trout. Afferent neural activity from O2 receptors in the first gill arch increased in response to hypoxic perfusate and NaCN. Adrenergic agonists (epinephrine, norepinephrine and isoproterenol) had little effect on neural activity. Dopamine and 5-hydroxytryptamine (serotonin) caused a brief, small burst in chemoreceptor activity followed by a mild inhibition of receptor discharge. Acetylcholine and nicotine were potent neurochemical stimulants; muscarine had only a slight effect. While atropine completely blocked the effects of acetylcholine on receptor discharge, it only slightly inhibited responses to hypoxia and NaCN. Thus, although cholinergic mechanisms appear more likely than either adrenergic or serotonergic mechanisms to alter cardiovascular and ventilatory reflexes in fishes through their effects on O2-sensitive chemoreceptor activity, the transduction process involved in O2-chemoreception appears to be complex and not dependent on any single one of the neurochemicals tested.

Adrenergic Antagonists↗

PubMed1982

Renorenal reflexes in the rat elicited upon stimulation of renal chemoreceptors.

The effects of renal ischemia and backflow of non-diuretic urine into the renal pelvis on renal efferent sympathetic postganglionic nerve activity, femoral arterial pressure and heart rate were studied to verify whether stimulation of renal chemoreceptors elicits autonomic reflexes. In rats with intact spinal cord or spinal cord sectioned at the T6 level a brief activation of renal chemoreceptors produced excitatory ipsilateral and contralateral renorenal reflexes, whereas it only slightly and insignificantly altered arterial pressure and heart rate. These results indicate that stimulation of renal chemoreceptors elicits renorenal excitatory reflexes which might be integrated both at spinal and supraspinal levels.

Adrenergic Fibers↗

PubMedDate not supplied

Split medulla preparation in the cat: arterial chemoreceptor reflex and respiratory modulation of the renal sympathetic nerve activity.

The study was undertaken in order to assess the changes in sympathetic output in a split medulla preparation of the cat which, as shown earlier, has impaired respiratory rhythm generation. The effects of medullary midsagittal sections on renal sympathetic nerve firing were investigated in chloralose anesthetized, paralyzed and artificially ventilated cats. Recordings of phrenic and recurrent laryngeal nerve activity served as indices of central respiratory rhythm generation. Sections, 5 mm deep from the dorsal medullary surface and extending 6 mm rostrally and 3 mm caudally to the obex, did not produce any significant changes in heart rate, blood pressure or tonic renal sympathetic nerve firing levels. They decreased or abolished, however, the respiratory rhythmicity in renal sympathetic nerve which paralleled the reduction of inspiratory discharges in phrenic and recurrent laryngeal nerves, and abolished the carotid body chemoreceptor-sympathetic reflex. The inspiratory activity remaining after the sections could still be enhanced by chemoreceptor stimulation. The inhibitory baroreceptor and pulmonary stretch receptor sympathetic reflexes, and the central excitatory effect of CO2 on renal sympathetic nerve firing were not altered. The effects of electrical stimulation within the midsagittal plane of the medulla have shown that descending pathways from the medullary inspiratory neurons (or their medullary collaterals) do not participate in the facilitation of spinal preganglionic neurons during inspiration and in relaying the pulmonary stretch receptor inhibitory sympathetic reflex. A region located close to the obex was identified from which excitatory responses in renal sympathetic nerves, compatible with the response obtained by carotid sinus nerve stimulation, could be evoked. It is concluded that a lesion in the midline of the lower medulla at the level of the obex selectively destroys cells or pathways which relay the carotid body chemoreceptor-sympathetic reflex.

Animals↗

PubMed1987

Ganglioglomerular nerves respond to moderate hypoxia independent of peripheral chemoreceptors in the cat.

The responses of the ganglioglomerular nerve (GGN) to transient changes and steady-state levels of paO2 at a constant paCO2 were studied in 12 anesthetized and spontaneously breathing cats before and after bilateral section of aortic (AN) and carotid sinus nerves (CSN). In two of these cats carotid chemoreceptor activity was monitored simultaneously. Onset of moderate hypoxia, down to paO2 of about 50 Torr, stimulated GGN activity and withdrawal of the hypoxic stimulus promptly eliminated the responses both before and after CSN section. CSN section, however, significantly raised the baseline activity and slightly delayed the GGN response to the onset of hypoxia. These responses to hypoxia are qualitatively similar to the characteristic responses of peripheral chemoreceptors. Thus, the basic oxygen chemosensing mechanism appeared to be present in the sympathetic nervous system, and is expressed in the postganglionic GGN activity. This property allows the sympathetic nervous system to perform physiologically important functions independent of the peripheral chemoreceptors.

Animals↗

PubMed1991

Responses of rostroventrolateral medulla spinal vasomotor neurones to chemoreceptor stimulation in rats.

The activity of spinal projecting 'vasomotor' neurones of the rostroventrolateral medulla (RVL) has been recorded in anaesthetised and paralysed rats. They responded to carotid body chemoreceptor stimulation (0.208 M NaH2PO4) with an increase in discharge that preceded an evoked increase in arterial blood pressure. This initial excitatory response was followed by a fall in discharge correlated to the rise in blood pressure. RVL neurones, which had equivalent sensitivity to baroreceptor inputs but no spinal projecting axons, failed to exhibit the initial excitatory response on chemoreceptor stimulation. These observations suggest that the pressor response to chemoreceptor stimulation is mediated, at least partially, by excitation of RVL-spinal 'vasomotor' neurones.

Animals↗

PubMed1981

Metabolic regulation of aortic chemoreceptor responses to CO2.

Modification of the unusually feeble responses of aortic chemoreceptors to CO2 was studied in cats which were anethetized, paralyzed, artificially ventilated and maintained at 38 degrees C. The inhibitor of oxidative phosphorylation, oligomycin, strikingly augmented the initial responses to CO2 of aortic chemoreceptors just as for carotid chemoreceptors, indicating that the basic mechanism of chemoreception might be regulated in part through energy metabolism.

Acetazolamide↗

PubMed1990

Chemoreceptor responses to substance P, physalaemin and eledoisin: evidence for neurokinin-1 receptors in the cat carotid body.

Substance P (SP) belongs to a group of peptides called tachykinins. Biological effects of SP are mediated by tachykinin receptors that have been classified as neurokinin-1 (NK-1), NK-2 and NK-3 subtypes. The aim of the present study is to elucidate the tachykinin receptor subtype(s) that mediate the excitatory effects of SP in the carotid body. For this purpose, we compared the carotid body responses elicited by SP with that of physalaemin and eledoisin. In other tissues, physalaemin exhibits equi or greater potency at NK-1 receptors and eledoisin exerts its effects more on NK-2 and NK-3 subtypes compared to SP. Experiments were performed on eight cats that were anaesthetized, paralyzed and artificially ventilated with room air. Close carotid body administration of SP and physalaemin produced dose-dependent augmentation of the chemoreceptor afferent activity. Chemoreceptor discharge, however, was unaffected by eledoisin. Compared to that by SP, the magnitude of excitation produced by physalaemin was the same at lower doses but significantly greater with the highest dose (100 nmol). The time course of the response induced by physalaemin, however, was the same as that by SP. The present results demonstrate that in the carotid body physalaemin is also either equi or relatively more potent than SP, whereas eledoisin has no effect on the chemoreceptor discharge. It is suggested that stimulation of the carotid body by SP is mediated by NK-1 but not NK-2 or NK-3 receptors.

Animals↗

PubMed1995

Basic fibroblast growth factor regulates ionic currents and excitability of fetal rat carotid body chemoreceptors.

Basic fibroblast growth factor (bFGF) and nerve growth factor (NGF) are known mitogens and/or differentiation factors for cells of the sympathoadrenal lineage. Though carotid body (CB) chemoreceptors (type 1 cells) are considered part of this lineage, their response to bFGF is unknown and so far they appear unresponsive to NGF in vitro. In this study we use whole-cell recording to investigate whether bFGF (and NGF) can influence the development of ionic currents in these chemoreceptors, cultured from fetal (E18-19) rat pups. bFGF (10ng/ml) significantly augmented both transient inward Na+ and outward K+ currents in type 1 cells after only 2 days of treatment; after normalizing for the accompanying increase in cell size, as indicated by whole-cell capacitance, the Na+ current density was nonetheless increased by bFGF. Unlike controls, bFGF-treated type 1 cells readily fired action potentials following depolarization. These effects were not mimicked by NGF (100 ng/ml) treatment. Since the carotid body is one of the most richly vascularized organs and bFGF is a potent angiogenic factor, it is conceivable that variations in local bFGF concentrations during fetal development may contribute to the known species differences in CB chemoreceptor excitability.

Animals↗

PubMed1988

Activation of hypothalamic arcuate but not paraventricular neurons following carotid body chemoreceptor stimulation in the rat.

The effect of carotid body chemoreceptor stimulation on 292 neurons in midline hypothalamic nuclei has been examined electrophysiologically in ethyl carbamate/sodium pentobarbitone anaesthetized rats. Experiments demonstrated that specific stimulation of carotid body chemoreceptors activates a small group (16) of neurons in the mediobasal hypothalamic arcuate nucleus, but has no effect on neurons (157) in the hypothalamic paraventricular nucleus or the anterior hypothalamus. Of 16 arcuate neurons activated by the stimulus, six projected to the median eminence and three projected to the dorsal medulla, as defined by antidromic invasion. Three of the neurons activated from the carotid body also showed a resting discharge that was linked with ventilation rate, suggesting that the arcuate nucleus may have some involvement with respiratory processing. The activation of neurons projecting to the median eminence implies that the release of adenohypophyseal hormones may also be influenced by carotid body chemoreceptors.

Animals↗

PubMed1996

Ventral medullary neuronal responses to peripheral chemoreceptor stimulation.

Recent findings suggest that carotid chemoreceptor input into the ventral medullary surface intermediate area during hypoxia is inhibitory (Gozal et al., (1994) Neurosci. Lett. 178, 73-76. However, systemic hypoxia is a complex stimulus, and effects of carotid chemoreceptor stimulation per se on intermediate ventral medullary surface neuronal activity are difficult to isolate. Therefore, we studied neural activation of the intermediate ventral medullary surface during peripheral chemoreceptor stimulation by intravenous sodium cyanide using optical procedures in seven pentobarbital-anesthetized cats. Control recordings were also acquired in the suprasylvian cortex of three cats. Images of reflected 660 nm light were collected at l/s with a charge-coupled device camera, triggered by the cardiac R wave, after 0.0, 0.5, 2, 5, 10, 20 and 40 micrograms/kg i.v. sodium cyanide administration before and following carotid sinus denervation. Sodium cyanide doses > 5 micrograms/kg significantly increased ventilation, an effect which was eliminated following carotid sinus denervation. A pronounced, dose-dependent activity decrease within the intermediate ventral medullary surface occurred within seconds of sodium cyanide administration, with subsequent return to baseline. Carotid sinus denervation eliminated rapid-onset neural responses to all sodium cyanide doses. However, at the 40 micrograms/kg dose, a smaller, slower onset (25 s), activity decrease occurred both pre- and postdenervation. In the neocortex, the sodium cyanide-induced fast responses were absent. Intravenous cyanide, acting via a carotid sinus nerve pathway, results in a dose-dependent decrease in neural activity within the intermediate ventral medullary surface of cats. High-dose sodium cyanide also appears to decrease intermediate ventral medullary surface neural activity directly.

Animals↗