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PubMed1989

Peptidergic innervation of arterial chemoreceptors.

The peptidergic innervation of arterial chemoreceptor organs (the rat carotid body and vagal paraganglia; guinea pig carotid body) was studied immunohistochemically. Five different populations of nerve fibres in the guinea pig carotid body could be discriminated according to their origin and their chemical coding. The innervation pattern of the rat carotid body differed in some aspects. Comparison of the rat carotid body and vagal paraganglia suggested that autonomic neuropeptide Y-like immunoreactive fibres act primarily via vascular mechanisms rather than directly on the chemoreceptor tissue. Sensory fibres were shown to contain immunoreactivities for substance P, calcitonin gene-related peptide (rat and guinea pig) and somatostatin (guinea pig). The functional role of the identified peptide-containing sensory fibres remains to be established.

Animals↗
PubMed1979

Arterial and cardiopulmonary baroreceptor and chemoreceptor influences and interactions on ear sympathetic nerve discharge in the rabbit.

1. The effects of changing intravascular pressures on integrated ear sympathetic nerve activity (ESNA) were studied in anesthetized artificially ventilated rabbits by inflating aortic and inferior vena caval perivascular balloons under conditions of normal arterial Po2 and during arterial hypoxia. 2. At normal Po2 ESNA was unaffected by arterial and cardiopulmonary baroreflex influences. The small inhibition of ESNA observed during rises in arterial pressure after vagotomy was also present after section of the carotid sinus and aortic nerves, and after cutting both vagi as well. 3. During hypoxia there was marked inhibition of ESNA, which was minimally influenced by vagotomy but abolished by section of the carotid sinus and aortic nerves, suggesting that it was chemoreceptor-mediated. There was a pressure-related rise in ESNA which was abolished by vagotomy and considered to be due to a central nervous chemoreceptor-cardiopulmonary baroreflex interaction.

Animals↗
PubMed1982

Ventilatory response to CO2 after brief stimulations of the peripheral chemoreceptors in man.

Whether or not stimulation of the peripheral chemoreceptors by hypercapnic-hypoxic exposure results in a long-lasting increase in ventilatory activities was studied using the steady state CO2 response test on 12 human subjects. The degree of hypercapnic hypoxia was end-tidal PCO2 (PETCO2) 42.1 +/- 3.0 and PO2 (PETO2) 39.8 +/- 4.7 mmHg, lasting for 5 min. Minute ventilation values at PETCO2 45 mmHg (V45) and PETCO2 at minute volume 15 liter . min-1 (P15) were calculated from the respective CO2 response curves. The differences in V45 and P15 between the control and the 30 min test group were found to be significant (p less than 0.05). These results suggested the left- and upward-shift of the CO2 response curve of the 30 min test group. On the other hand, in 5 of the 12 subjects, three successive CO2 response tests conducted at 0, 30, and 90 min without hypercapnic-hypoxic exposure showed fairly reproducible results, and no statistically significant differences were found between any of the above trials with the parameters S, B, V45, and P15. These results indicated that the CO2 response curve obtained by using the steady state method can be effected for at least 30 min even if the stimulation of the peripheral chemoreceptors is only for brief periods.

Adolescent↗
PubMed1992

Evidence for phase-locking response to hypoxia in peripheral chemoreceptor activity in man.

A number of animal studies have demonstrated that the ventilatory response to stimulation of the peripheral chemoreceptors is well reproduced only when it is stimulated during inspiratory period. In humans, such a response has not been confirmed when using a mild hypoxic stimulus. We, therefore, hypothesized that this response may be detected when a more intense hypoxia is applied. To confirm this hypothesis, six healthy subjects inhaled N2 gas mixture with 5% CO2 in an amount of vital capacity. This procedure started from steady state mild hypoxia (PET02; 60-70 mmHg). Inspiratory and expiratory minute ventilation (VI and VE), tidal volume (VT), and inspiratory and expiratory time (TI and TE) of the breath, at the start of falling oxygen saturation, were analyzed. 21% O2 + 5% CO2 balanced with N2 was inhaled and a breath cycle with a similar latency as during N2 gas mixture inhalation was also analyzed as a control. When oxygen saturation began to drop at the inspiratory phase, the increment of ventilation and tidal volume were larger than the control. When it occurred at the expiratory phase, no significant difference from the control was seen. These results signify the presence of rectification of chemoreceptor afferent signal in humans and may support the concept of oscillation hypothesis as an effective ventilatory stimulus.

Adult↗
PubMed1995

Different effects of removing extracellular Ca2+ on cytosolic Ca2+ response to anoxia of sensory neurons and carotid chemoreceptor cells from newborn rabbits.

To study the mechanism of the increases in cytosolic Ca2+ ([Ca2+]i) induced by anoxia, the author examined the effect of removing extracellular Ca2+ on the [Ca2+]i response in cultured nodose ganglion neurons (control) and carotid body glomus cells prepared from newborn rabbits using a fura-2 microfluorimetry. The sensory neurons showed a small increase in [Ca2+]i during anoxia which was not affected by the removal of extracellular Ca2+ or D600. On the other hand, in the chemoreceptor glomus cells, Ca2+ removal eliminated the anoxia-induced large [Ca2+]i increase in 85% of the tested cells (n = 67), and depressed it in the rest. Interestingly, recovery from exposure to an anoxic Ca(2+)-free solution reversibly produced a large and transient rise in [Ca2+]i. The magnitude of this post-anoxic/Ca(2+)-free [Ca2+]i transient correlated with the intensity of the suppression of the [Ca2+]i response to anoxia in Ca(2+)-free solution. Also the [Ca2+]i transient was mostly inhibited by L-type Ca2+ channel blockers (nifedipine and D600), but was not affected by tetrodotoxin. These results suggest that the anoxia-induced large increase in [Ca2+]i were, in most glomus cells, coming from extracellular sources and, in a few cells, from both extracellular sources and from intracellular pools, whereas the slight increase in [Ca2+]i in sensory neurons was probably produced by releasing Ca2+ from intracellular stores. The post-anoxic/Ca(2+)-free [Ca2+]i transient, seen in the chemoreceptor cells alone, may have resulted from modification of the anoxic [Ca2+]i response by Ca2+ removal and involves mostly L-type Ca2+ channels and a few other Ca2+ entry pathways.

Animals↗
PubMed1977

Interaction between vagal and chemoreceptors afferents in ventilatory response to transient hypercapnia (anaesthetized rabbit).

In rabbits anaesthetized with ethyl-carbamate, stimulation of chemoreceptors afferents was allowed by transient hypercapnia, before and after vagal blockade by DC current. In these relatively fast breathing animals, the transient hypercapnia produced light changes of inspiratory tidal volume (VI), inspiratory (TI) and expiratory durations (TE). Despite the identity of transient hypercapnia, it ensued that: (1) the higher the spontaneous VI and the lower the respiratory frequency (fR), the greater their respective changes (deltaVI and deltafR) during the ventilatory response; (2) after vagal blockade, greater changes in VI, TI, TE and mean inspiratory flow rate (VI/TI) occurred than in control state, while the relation between deltafR and fR was more significant than in control state. Respective roles played by vagal and chemoreceptors afferents in the ventilatory response to transient hypercapnia are discussed.

Animals↗
PubMed1978

Interaction between vagal and chemoreceptors afferents in ventilatory response to transient hypercapnia (awake rabbits).

The ventilatory response to a transient hypercapnia was studied in four awake rabbits maintained in a volume displacement plethysmograph : the increase in inspiratory volume (VI) was associated or not with an increase in inspiratory and expiratory durations (TI and TE). These ventilatory variations were consistent with the activation of the peripheral chemoreceptors by carbon dioxide (short latency of the initial response). After vagal blockade by local anaesthesia, relative ventilatory variations were not significantly different from those previously measured. Central activity seems an important factor reducing inhibitory vagal input and favouring peripheral chemoreceptor afferents.

Afferent Pathways↗
PubMed2005

Chemical and electric transmission in the carotid body chemoreceptor complex.

Carotid body chemoreceptors are complex secondary receptors. There are chemical and electric connections between glomus cells (GC/GC) and between glomus cells and carotid nerve endings (GC/NE). Chemical secretion of glomus cells is accompanied by GC/GC uncoupling. Chemical GC/NE transmission is facilitated by concomitant electric coupling. Chronic hypoxia reduces GC/GC coupling but increases G/NE coupling. Therefore, carotid body chemoreceptors use chemical and electric transmission mechanisms to trigger and change the sensory discharge in the carotid nerve.

Animals↗
PubMed1997

[Effects of NPY microionophoresis on the units in nucleus tractus solitarius (NTS) responsive to baro- and chemoreceptor].

This experiment is designed to study the effects of NPY microionophoresis on the units in NTS responsive to baro- and chemoreceptor activiation at cellular level. In the experiment, it examined 62 units with spontaneous discharge in NTS. Among them, 34 were excited and 19 were inhibited by NPY microionophoresis. And other 9 units failed to respond to NPY microionophoresis. The units with the increase and decrease of discharge frequency to the activation of carotid baroreceptor showed excitation (16/21) and inhibition (7/11) respectively in response to NPY microionophoresis. The units with the increase (8/14) and decrease (5/9) of discharge frequency to the activation of carotid chemoreceptor mainly showed excitation.

Animals↗
PubMed1999

Reflex changes in heart rate during chemoreceptor stimulation in monkeys.

The changes in heart rate induced by the stimulation of arterial chemoreceptors by apneic asphyxia and left atrial - intracarotid injections of sodium cyanide were investigated in anesthetized artificially ventilated and paralysed monkeys. Apneic asphyxia and sodium cyanide injection caused tachycardia, bradycardia, or both in monkeys paralysed with decamethonium bromide and tachycardia only, in monkeys paralysed with gallamine. In both groups, the tachycardia was abolished by prior administration of propranolol and the bradycardia, by atropine. Prior ventilation with 100% O2 abolished the heart rate responses produced by apnea. Recording of phrenic efferent activity showed that the neural discharge increased in response to apneic asphyxia and sodium cyanide injections. It remained so during the manifestation of tachycardia, bradycardia, or no change in heart rate, suggesting that even though "higher centres" may have an important influence in the heart rate responses elicited, central respiratory drive may not be the only mechanism. The present results show that in the nonhuman primate, arterial chemoreceptor stimulation elicits both cardioacceleratory and cardioinhibitory reflexes, and the net effect of their stimulation on heart rate depends upon the balance between these opposing mechanisms.

Adrenergic beta-Antagonists↗
PubMed2001

Oxygen sensitive chemoreceptors in the first gill arch of the tadpole, Rana catesbeiana.

Spike frequency was recorded in the nerve of the isolated superfused first gill arch of the bullfrog larva, Rana catesbeiana and the response to different superfusate PO2 was evaluated. In the metamorphic tadpole, spike frequency increased significantly when the superfusate PO2 was decreased (mean +/- SEM): 8.5 +/- 1.6 Hz at 650 Torr, 11.7 +/- 1.9 Hz at 140 Torr, 13.3 +/- 1.8 Hz at 65 Torr, 14.8 +/- 2.4 Hz at 0 Torr (ANOVA, p = 0.0002). The O2 sensitive chemoreceptor stimulants NaCN and almitrine also increased the spike frequency. This study demonstrates the presence of O2 sensitive chemoreceptors in the first gill arch of the tadpole.

Animals↗
PubMed1975

[Kidney function and arterial acid-base status during continuous stimulation of the carotid chemoreceptors in vagotomized cats].

In spontaneously breathing, chloralose narcotized and bilaterally vagotomized cats under mannite saline diuresis, the isolated carotid sinus were perfused for 1 hr with arterial and then for 1 hr with venous blood, and subsequently again with arterial blood for 1 hr. Either measure d or calculated were the parameters of arterial acid-base status, the arterial systemic bl-od pressure, the p-aminohippuric acid (PAH), inulin (IN), and osmolar clearance, the filtration fraction, the tubular reabsorption of oxmotically free water, the urinary time volume, and fractional excretions of the kidneys. Stimulation of the carotic chemoreceptors increased respiration, slightly enhanced the CPAH, and caused a minor fall of CIN with little altered filtration fraction. The renal resistance increased. The absolute and fractional excretions of urine, sodium, potassium, and of osmotically active particles rose significantly. Tubular reabsorption of osmotically free water showed a singificant increase. Urinary osmolarity remained constant in general. The changes of water and electrolyte excretion did not correlate with those of renal hemodynamics. The results argue against natriuresis being caused on chemoreceptor stimulation by increased filtrate volume of the whole kidney, or by decreased osmolarity of the renal medulla. The results are discussed with regard to the renal function in arterial oxygen deficiency.

Acid-Base Equilibrium↗
PubMedDate not supplied

[Central chemoreceptors and sudden infant death syndrome].

INTRODUCTION: Carbon dioxide partial pressure and pH in the extracellular compartment are the most powerful signals regulating respiration. Central chemoreceptors (QC) undergo the stimulating effect of CO2 and pH upon respiration. AIMS: This review tries to provide an actual envision of the progress in the knowledgement on central chemoreception. It also tries to highlight the importance of the alterations in the chemoreception mechanism as a cause of sudden infant death syndrome (SIDS). DEVELOPMENT: Central chemoreceptors respond to acid-base imbalance acting on neurons that give rise to the central breathing pattern and have the ability to change the respiratory rate, which is normally needed to restore the normal values of acid-base status. QC are widely distributed in the brain stem, however QC neurons in the ventral surface of the medulla like to be the main relays for ventilatory responses after acid-base stimulation. CONCLUSIONS: It has been shown that QC are sensitive to pH and CO2 as in vivo as in vitro conditions, most of them being serotonin immunopositive, a neurotransmitter with known effects on breathing pattern. By other side, alterations of central chemoreception have been associated to pathologies like congenital hypoventilatory syndrome or SIDS. Interestingly, the post mortem exams of the brain of infants dead because these syndromes have showed anomalies of serotonergic receptor located in regions containing QC neurons and in others related with cardiorespiratory integration.

Carbon Dioxide↗
PubMed1991

Natriuresis secondary to carotid chemoreceptor stimulation with almitrine bismesylate in the rat: the effect on kidney function and the response to renal denervation and deficiency of antidiuretic hormone.

Almitrine bismesylate simulates the effects of arterial hypoxia in producing a specific and long-lasting excitation of the peripheral arterial chemoreceptors. Previous work has shown that almitrine produces a diuresis and natriuresis when given intravenously to anaesthetised rats in a stable mannitol induced diuresis. This response is abolished by glossopharyngeal nerve section implying that it is afferently mediated via the carotid body chemoreceptors. We have studied further the efferent limb of this response. The diuresis and natriuresis occurs without significant detectable changes in effective renal plasma flow and glomerular filtration rate suggesting that it is produced mainly by inhibition of renal tubular sodium and water reabsorption. Almitrine produces a diuresis and natriuresis in rats after bilateral nephrectomy and transplantation of a kidney from a donor rat. This effect is not therefore efferently mediated by the renal nerves and probably involves a humoral agent. Almitrine produces a diuresis and natriuresis in rats after bilateral adrenalectomy and in rats with congenital hypothalamic diabetes insipidus indicating that neither adrenal hormones nor changes in antidiuretic hormone levels are implicated.

Almitrine↗
PubMed1989

The glomus tympanicum: a middle ear chemoreceptor?

Negative pressure in the middle ear has been identified as an important factor in the pathogenesis of middle ear disease. Unfortunately, to date, the physiological mechanisms that control middle ear pressure are poorly understood. Recent interest has focused on the possible role of carotid body-like tissue in the middle ear (the glomus tympanicum) as a chemoreceptor for changes in the gas composition of the middle ear. From the few anatomical studies of normal glomus tissue in the temporal bone it would seem that glomus bodies may not be consistently present in the middle ear. In this study, glomus bodies were sought in histological preparations of the promontory mucosa and tympanic plexus. It was found that the glomus tympanicum is only occasionally present in the middle ear mucosa, and thus a chemoreceptor role specific to the middle ear is unlikely.

Chemoreceptor Cells↗
PubMed1987

Effect of almitrine on renal sodium excretion in chemoreceptor denervated spontaneously hypertensive rats.

The effect of almitrine on urinary sodium excretion was investigated in conscious carotid body-, sino-aortic- and sham-denervated SHR. The animals were kept singly in metabolic cages and had free access to food and tap water. Oral application of almitrine (0.5 mg/kg bwt) during five days induced a twofold natriuresis in sham-operated rats. The first natriuretic response on the fourth day of almitrine treatment was observed in animals of all groups indicating that this effect is not chemoreceptor mediated. The second natriuresis seen on the sixth day of the post-treatment period in both sino-aortic and sham-operated SHR but not in the carotid-body denervated rats does not permit clear conclusions to be drawn. We tend to assume that the natriuretic action of almitrine is not chemoreceptor mediated in conscious SHR.

Almitrine↗
PubMed1987

Influence of infusion of deoxycorticosterone acetate on the responses of kidney function elicited by stimulation of the peripheral arterial chemoreceptors with almitrine bismesylate in anaesthetized rats.

In two groups of male, normotensive, spontaneously breathing rats in chloralose-urethane anaesthesia the peripheral arterial chemoreceptors were stimulated by intravenous infusion of almitrine bismesylate (0.25 mg/kg). The experiments were carried out in moderate osmotic diuresis. In one series desoxycorticosterone acetate (DOCA) was infused at a rate of 35-40 ng/min.100 g body weight. Urine was collected via a bladder catheter. Kidney hemodynamics as well as tubular and excretory function were determined using the clearance-technique. In both groups of animals administration of almitrine caused an increase of breathing rate as well as an increase of the oxygen tensions and the pH-values in the arterial blood. Mean systemic arterial blood pressure, effective renal plasma flow and glomerular filtration rate decreased slowly with the time of the experiments, whereas renal hemodynamic resistance tended to increase both in the control and in the DOCA treated group. In both groups of animals intravenous infusion of almitrine was followed by an inhibition of renal tubular sodium reabsorption and an increase of both the absolute and the fractional salt excretion. The data indicate that arterial chemoreceptor stimulation in rats causes an inhibition of renal tubular sodium reabsorption which does not result from a reduced tubular action of mineralocorticoid hormones.

Almitrine↗