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PubMed1994

ANTAGONISTIC FREQUENCY TUNING OF HAIR BUNDLES BY DIFFERENT CHEMORECEPTORS REGULATES NEMATOCYST DISCHARGE

Sea anemones capture prey by discharging nematocysts into them. Chemical and mechanical cues identify suitable prey to sensory receptor systems on the anemone. Conjugated N-acetylated sugars from prey bind to chemoreceptors on cnidocyte/supporting cell complexes to tune hair bundles on the complexes to lower frequencies matching prey movements. The hair bundles regulate discharge of microbasic p-mastigophore nematocysts into vibrating targets. Provided that proline receptors are activated after those for N-acetylated sugars, nematocyst discharge is tuned to much higher frequencies. Thus, anemone hair bundles are tuned to either higher or lower frequencies by antagonistic chemoreceptors. Chemoreceptors for proline can adapt to 10(-8) mol l-1 proline and yet respond to increases in proline concentration of less than 10(-15) mol l-1. Under these conditions, too few molecules of proline are added to activate chemoreceptors on all responding cnidocyte/supporting cell complexes. Evidence indicates that the extreme sensitivity of anemones to proline may be attributed, in part, to intercellular communication.

Journal Article↗

PubMed2002

Postnatal hypoxemia increases angiotensin II sensitivity and up-regulates AT1a angiotensin receptors in rat carotid body chemoreceptors.

In the present study, the effects of postnatal hypoxemia on the AT1 angiotensin receptor-mediated activities in the rat carotid body were studied. Angiotensin II (Ang II) concentration-dependently increased the chemoreceptor afferent activity in the isolated carotid body. Single- or pauci-fiber recording of the sinus nerve revealed that the afferent response to Ang II was enhanced in the postnatally hypoxic carotid body. To determine whether the increased sensitivity to Ang II is mediated by changes in the functional expression of Ang II receptors in the carotid body chemoreceptors, cytosolic calcium ([Ca2+]i) was measured by spectrofluorimetry in fura-2 acetoxymethyl ester-loaded type I cells dissociated from carotid bodies. Ang II (25-100 nM) concentration-dependently increased [Ca2+]i in the type I cells. The proportion of clusters of type I cells responsive to Ang II was higher in the postnatally hypoxic group than in the normoxic control (89 vs 66%). In addition, the peak [Ca2+]i response to Ang II was enhanced 2- to 3-fold in the postnatally hypoxic group. The [Ca2+]i response to Ang II was abolished by pretreatment with losartan (1 microM), an AT1 receptor antagonist, but not by PD-123177 (1 microM), an AT(2) antagonist. Double-labeling immunohistochemistry confirmed that an enhanced immunoreactivity for AT1 receptor was co-localized to the lobules of type I cells in the hypoxic group. In addition, RT-PCR analysis of subtypes of AT1 receptors showed an up-regulation of AT1a but a down-regulation of AT1b receptors, indicating a differential regulation of the expression of AT1 receptor subtypes by postnatal hypoxia in the carotid body. These data suggest that postnatal hypoxemia is associated with an increased sensitivity of peripheral chemoreceptors in response to Ang II and an up-regulation of AT1a receptor-mediated [Ca2+]i activity of the chemoreceptors. This modulation may be important for adaptation of carotid body functions in the hypoxic ventilatory response and in electrolyte and water homeostasis during perinatal and postnatal hypoxia.

Angiotensin II↗

PubMed1975

Response of muscular and cutaneous vessels to physiologic stimulation of chemoreceptors (38505).

Experiments were performed to determine whether physiologic stimulation of carotid chemoreceptors produces different responses in blood vessels of skin and muscle. Carotid chemoreceptors of anesthetized dogs were stimulated with hypoxic and hypercapnic blood and responses were observed in the isolated, perfused gracilis muscle and hindpaw. Chemoreceptor stimulation produced vasoconstriction in the muscle and vadodilatation in the paw (a predominantly cutaneous vascular bed). Responses to hypoxia without hypercapnic acidosis tended to be less pronounced. The study indicates that physiologic stimulation of carotid chemoreceptors produces contrasting responses in different vascular beds.

Acidosis↗

PubMed1981

The neural pathway involved in "efferent inhibition" of chemoreceptors in the cat carotid body.

This study was done to determine whether a pathway of efferent axons in the carotid sinus nerve is necessary for the phenomenon of "efferent inhibition" (inhibition induced in carotid body chemoreceptors by electrical stimulation of the carotid sinus nerve). Our approach was to eliminate efferent axons in the carotid sinus nerve of cats without destroying the sensory axons. This was achieved by cutting the ipsilateral glossopharyngeal and vagus nerves central to their sensory ganglia and/or by removing the nodose and superior cervical ganglia. In neurophysiological studies we found that the response of chemoreceptors in cats 10 days after surgery was the same as that in controls. chemoreceptor activity was decreased by electrical stimulation of the carotid sinus nerve and was increased by hypoxia and cyanide. In operated cats as in control animals, "efferent inhibition" was abolished by haloperidol and dihydroergotamine, drugs that block the inhibitory action of dopamine. Electron microscopic studies disclosed that the number of nerve endings in glomus cell/sheath cell complexes was not measurably different in control and experimental carotid bodies. By contrast, 10 days after the carotid sinus nerve was cut the number of nerve endings next to such ells was reduced by more than 99%. cutting the nerve roots and excising the ganglia eliminated most nerve endings on blood vessels: The number of noradrenergic-type nerve endings was reduced 99% and other types of nerve endings (presumptive cholinergic and peptidergic types) were reduced by more than 90%. Our experiments indicate that "efferent inhibition" is not abolished by operations that destroy inputs to blood vessels and to carotid boy glomus cells from (1) the nodose ganglion, (2) superior cervical ganglion, or from (3) neurons in the brain stem whose axons run in the glossopharyngeal or vagus nerves. We conclude that " efferent inhibition" may be caused by antidromic stimulation of sensory axons.

Animals↗

PubMed2002

Electrical properties of chemoreceptor elements in the carotid body.

The electrical properties of chemoreceptor afferent nerve fibers and glomus cells and the behavior of cytosolic Ca(2+) in glomus cells are reviewed. While this has not been confirmed, spontaneously depolarizing potentials (SDPs) recorded in a chemoreceptor afferent terminal may be the postsynaptic expression of presynaptic events. Glomus cells, which are presynaptic elements, either depolarized or hyperpolarized in response to natural and chemical stimulation. After-hyperpolarization following an initial depolarization and after-depolarization following an initial hyperpolarization were often seen. When a glomus cell depolarizes, voltage noise increases despite a decrease in input resistance in both intact and denervated carotid bodies. The voltage noise may be "receptor noise" generated in the glomus cell itself. The electrical properties of glomus cells change in the denervated carotid body, which suggests that the chemoreceptor afferent nerve exerts some trophic effect(s) on glomus cells. Hypoxia either increases or decreases cytosolic Ca(2+), while ACh or NaCN induces either an increase or no change in cytosolic Ca(2+) in glomus cells. There are at least two possible explanations for voltage changes in glomus cells: a chemical stimulus first depolarizes the glomus cell and induces Ca(2+) influx to release chemical substances, or a chemical stimulus induces an increase in [Ca(2+)](i) and then hyperpolarizes the glomus cell via potassium influx.

Carotid Body↗

PubMed1982

Arterial chemoreceptor inhibition by a single inspirate containing carbon monoxide is accounted for by raised arterial PO2.

Carbon monoxide (CO) slugs (10--100 ml) injected into the inspired air of 6 hypoxic, anaesthetized cats reduced carotid body chemoreceptor discharge. The inhibition was invariably associated with a sharp rise in Pa, O2 which was continuously recorded by a fast responding intravascular electrode. This suggests that CO in solution in the blood leaving the lungs displaces O2 from blood after it was left the exchange region and that the displaced O2 raises the Pa, O2 and inhibits chemoreceptor discharge. Our results provide no support for the idea that a haemoglobin-like pigment is involved in the mechanism of arterial chemoreceptor excitation.

Action Potentials↗

PubMed1983

Chemoreceptor sensitivity and maladaptation to high altitude in man.

Studies were carried out to find out the role of chemoreceptor sensitivity in the causation of maladaptation syndromes on acute exposure to altitude. The experiments were done in two phases. In phase I, the responses in chemoreceptor sensitivity were studied in altitude acclimatized subjects and compared with those who suffered from either High Altitude Pulmonary Oedema (HAPO) or Acute Mountain Sickness (AMS). In Phase II, a similar comparison was done in two groups of subjects, one representing normal sojourners at 3,500 m and the other being subjects who had just recovered from HAPO. The first phase was done at Delhi; and the second at an altitude of 3,500 m. Parameters of assessment were hypoxic sensitivity, carbon dioxide sensitivity, ventilation (VE), respiratory frequency (Rf), forced vital capacity (FVC), forced expiratory volume at the first second (FEV1), heart rate (HR), blood pressure (BP), and oral temperature (Tor). The results showed significantly lower sensitivity to both hypoxia and carbon dioxide in maladapted subjects, as compared to those who were acclimatized in both the categories suggesting thereby that reduced chemoreceptor sensitivity might be an initiating factor in the causation of maladaptation syndromes at altitude.

Adult↗

PubMed1999

The release of catecholamines in hypothalamus and locus coeruleus is modulated by peripheral chemoreceptors.

To investigate whether impulses from chemoreceptors influence the release of catecholamines in the hypothalamus and the locus coeruleus, the two brain areas were superfused simultaneously and bilaterally with artificial cerebrospinal fluid through push-pull cannulae. The release of catecholamines was determined in the superfusate before and during chemoreceptor stimulation by bicarbonate solution saturated with carbon dioxide (CO2-NaHCO3) or KCN. Experiments were carried out on intact cats after carotid body denervation (CD). Intracarotid infusion of CO2-NaHCO3 increased arterial blood pressure and enhanced the release of noradrenaline but not dopamine in the posterior hypothalamus and the locus coeruleus. Following CD, the enhancing effect of CO2-NaHCO3 on the noradrenaline release in the posterior hypothalamus was abolished, while the effect on blood pressure was slightly enhanced. CD reversed the NaHCO3-induced release of noradrenaline in the locus coeruleus to a decreased noradrenaline outflow. Intracarotid infusion of KCN led to a fall in blood pressure. KCN increased the release rates of noradrenaline and, to a lesser extent, that of dopamine in the posterior hypothalamus, as well as the release of noradrenaline in the locus coeruleus. CD abolished the KCN-induced fall of blood pressure and the increased release of noradrenaline and dopamine in the posterior hypothalamus. Similar to CO2-NaHCO3, the enhancing effect of KCN on the noradrenaline release in the locus coeruleus was reversed following CD to a reduced noradrenaline outflow. Superfusion of the posterior hypothalamus and the locus coeruleus with KCN did not influence either blood pressure or the release rates of noradrenaline and dopamine in these brain areas. The findings show that impulses originating from chemoreceptors of the carotid body increase the release rates of the catecholamines in the posterior hypothalamus and the locus coeruleus, thus underlining the importance of catecholaminergic neurons of these brain areas in cardiovascular control.

Animals↗

PubMed2003

Enhancement of carotid chemoreceptor reflex and cardiac chemosensitive reflex in the acute phase of myocardial infarction of the anesthetized rabbit.

In the acute phase of cardiac ischemia there is an imbalance of the autonomic outflow with a depression of the baroreceptor reflex. Carotid chemoreceptor stimulation evokes an increase on arterial blood pressure and bradycardia in the anesthetized and paralyzed animal. The activation of cardiac chemosensitive fibers elicit the Bezold-Jarisch reflex comprising a decrease of arterial blood pressure and bradycardia. In the present study, we studied the modifications of the carotid chemoreceptor reflex and the Bezold-Jarisch reflex elicited during the acute phase of myocardial infarction (MI) in the anesthetized and paralyzed rabbit. Rabbits were anesthetized with pentobarbitone, paralyzed and artificially ventilated. The carotid sinus region was exposed and a cannula was inserted retrogradely through the external carotid artery into the carotid bifurcation; the carotid body was stimulated by a lobeline injection. A catheter was advanced, via the right carotid artery, to the origin of the aorta and the Bezold-Jarisch reflex was evoked by an injection of ATP. The baroreflex was provoked by an increase in after-load or by clamping the common carotid artery. Heart ischemia was provoked by ligation of the descending coronary artery. Arterial blood pressure, carotid artery pressure, heart rate and electrocardiogram were monitored. Stimulation of cardiovascular and cardiac receptors was performed before and after coronary ligation. Results show an overall increase in the cardiovascular reflex responses elicited by stimulation of chemically activated receptors and an overall decrease of the baroreceptor responses after MI. In conclusion, these data show the existence of an enhancement of the reflex cardiovascular responses to carotid chemoreceptor and cardiac chemosensitive receptors stimulation and confirmed the depression of baroreceptor reflexes following heart ischemia that could account for the imbalance of the autonomic output observed in the acute phase of myocardial infarction.

Adenosine Triphosphate↗

PubMed2000

Developmental changes in chemoreceptor nerve activity and catecholamine secretion in rabbit carotid body: possible role of Na+ and Ca2+ currents.

In order to better understand the post-natal increase in peripheral chemoreceptor responsiveness to hypoxia, chemoreceptors of newborn (1-2 days) and older (10-12 days, 30 days, adult) rabbits were isolated and superfused, in vitro. The free tissue catecholamine concentration was measured using carbon-fiber voltammetry and pauci-fiber nerve activity was recorded from the sinus nerve during stimulation (4 min) with graded hypoxia or increased potassium. Both the peak catecholamine and peak nerve responses to stimulation with 10% and 0% oxygen increased with age, particularly between 10 and 30 days of age. In contrast, peak nerve and peak catecholamine responses to increased potassium did not significantly change with age. For a better understanding of how responsiveness increases with age, the fast Na+ and the Ca2+ currents were measured from isolated glomus cells of newborn and older rabbits, but the magnitude of the currents when normalized to membrane area was not significantly different between ages. We conclude that: (1) rabbit chemoreceptors mature in the newborn period (10-30 days) and part of this maturation is an increase in catecholamine secretion, (2) maturation of hypoxia transduction primarily occurs in steps prior to depolarization since potassium-evoked responses were not affected, and (3) an increase in the magnitude of glomus cell fast Na+ or Ca2+ currents is not a likely mechanism for the maturational change, but changes in the oxygen sensitivity of these currents cannot be excluded.

Age Factors↗

PubMed2003

Endogenous GABA in the commissural subnucleus of the NTS inhibits the carotid chemoreceptor reflex via GABA A receptors in rats.

Using urethane-chloralose anesthetized rats, we investigated which GABA receptor is responsible for the action of endogenous GABA on the carotid chemoreceptor reflex in the commissural subnucleus of the nucleus tractus solitarius (commNTS). Microinjection of the selective GABA uptake inhibitor nipecotic acid (40 nmol) into the commNTS attenuated the increases in respiration (respiratory movement and rate) and the elevation in arterial blood pressure elicited by carotid chemoreceptor stimulation. These effects were completely antagonized by premicroinjection of the GABA(A) antagonist bicuculline (20 pmol), but not of the GABA(B) antagonist 2-OH-saclofen (400 pmol), into the same site. These findings suggest that endogenous GABA mainly acts on GABA(A) receptors, and inhibits the chemoreceptor reflex in the commNTS in rats.

Animals↗

PubMed1982

Adaptive response of carotid body chemoreceptors to CO2.

Carotid body chemoreceptor responses to sudden changes in pETCO2 (end-tidal tracheal CO2 partial pressure) and paCO2 (arterial CO2 partial pressure) from one stable state to another at a constant level of PETO2 (end-tidal tracheal O2 partial pressure) and paO2 (arterial O2 partial pressure) were studied in 18 anesthetized cats. Chemoreceptor activity was recorded from single or pauci-fiber filaments of a cut sinus nerve. During a hypercapnic stimulus by CO2 inhalation the discharge rate rapidly increased to a peak and then adapted to a lower level in 20-30 s showing an overshoot in the response. Likewise, withdrawal of the hypercapnic stimulus was followed by an undershoot in chemoreceptor activity. Hypoxia decreased the latency of the response and increased the overshoot and stable state responses to hypercapnia. The responses to step paCO2 increases by blood perfusion were qualitatively similar but the latency and time to peak amplitude were shorter and the peak amplitude was larger at any given perfusate pO2. The stable state responses to a given paCO2 achieved by CO2 inhalation or by blood perfusion were similar. The transient overshoot and undershoot in the activity produced by the increase and decrease in paCO2 were blocked by acetazolamide, a carbonic anhydrase inhibitor. The results are best explained by postulating that in the carotid body tissue, H+ is generated from CO2 in one compartment in the presence of carbonic anhydrase and is transported to another containing the receptor site in a pO2 dependent way--a high pO2 attenuating and a low pO2 augmenting it.

Acclimatization↗

PubMed1989

Possible locations of pH-dependent central chemoreceptors: intramedullary regions with acidic shift of extracellular fluid pH during hypercapnia.

Using liquid membrane pH microelectrodes, we evaluated rapid and transient changes in extracellular fluid (ECF) pH within the medulla during vertebral artery injections of CO2-saturated saline (0.5 ml) in anesthetized (Dial-urethane), spontaneously breathing cats. We found intramedullary regions where ECF pH shifted to the acid side in the time course analogous to respiratory excitation during the CO2 loadings: the acidic shift occurred just before the respiratory excitation. Since most of the tested regions showed no or few changes in ECF pH, the responsive regions are thought to be specific local environments fitting the central chemoreceptors. Forty (85%) out of the 47 responsive regions were found to be scattered in the ventrolateral medulla, i.e. a long narrow zone extending from the ventrolateral surface to the ventral respiratory group (VRG) areas where inspiratory or expiratory activity was frequently recorded. The responsive regions were not necessarily restricted to the superficial ventral layers. We were also able to find the responsive regions in the dorsal area ventral to the nucleus tractus solitarii, though they were fewer in number (7/47). The distributions corresponded rougly to the areas where we had previously identified the tonically firing neurons excited exclusively by stimulation of the central chemoreceptors. These results indicate a possibility that the pH-dependent central chemoreceptors, if any, would be located within the regions demonstrated in this study.

Animals↗

PubMed1980

Long-lasting hyperventilation induced by almitrine: evidence for a specific effect on carotid and thoracic chemoreceptors.

In anesthetized dogs, almitrine (0.5-3 mg/kg i.v.) induced a dose-dependent increase in respiratory rate and ventilation. The aortic and carotid chemoreceptors were involved in the effects of almitrine. Section of both carotid sinus nerves and vagus nerves abolished the effects of the drug on respiration. The respiratory response did not occur in dogs with bilateral lesions of the nucleus of the solitary tract. The electrical activity of chemoreceptor fibres was increased. Perfusion of almitrine into the carotid artery stimulated respiration. Inhalation of pure oxygen shifted the dose-response curve of the respiratory effect towards the right. Almitrine slightly stimulated ventilation in dogs with bilateral section of carotid sinus nerves and aortic nerves and this disappeared when both vagus nerves were cut indicating that this effect was mediated through some chemoreceptor fibres present in the vagus nerves or through afferent vagal fibres.

Animals↗

PubMed1977

Response of avian intrapulmonary chemoreceptors to venous CO2 and ventilatory gas flow.

Avian intrapulmonary chemoreceptor activity is reduced by increasing airway PCO2 from 0 to 60 torr. Using extracellular electrodes, we recorded discharge of individual intrapulmonary chemoreceptor cell bodies in the left nodose ganglion of the rooster (Gallus domesticus) during unidirectional ventilation of the lungs. All receptors recorded were in the left lung. To vary pulmonary arterial PCO2 independently of ventilation, we ventilated the two lungs separately and supplied the left pulmonary circulation with systemic arterial blood. When the PCO2 in the pulmonary arterial blood was increased, discharge frequency decreased in all 21 receptors studied. Sensitivity to pulmonary arterial PCO2 was similar to sensitivity to airway PCO2. When PCO2 of ventilatory gas was lower than that of pulmonary arterial blood, discharge frequency of the receptor increased when pulmonary blood flow was stopped. Discharge frequency also increased when PCO2 at the receptor site was lowered by increased ventilatory gas flow. We conclude that intrapulmonary chemoreceptors respond to the delivery and removal of CO2 by blood and ventilatory gas. This suggests that the receptors are located within the respiratory gas exchange region of the lung. Because these receptors have a strong inhibitory effect on ventilation, they may serve to (1) adjust minute ventilation to the rate of metabolic CO2 production and (2) to regulate individual breath size.

Animals↗

PubMed1978

Intrapulmonary and systemic CO2-chemoreceptor interaction in the control of avian respiration.

Experiments on anesthetized chickens were conducted to study interactions between afferent activity from the intrapulmonary and systemic CO2-sensitive chemoreceptors in the generation of respiratory amplitude (RA) and respiratory frequency (f). The thoracoabdominal cavity was opened, air sacs ruptured and each lung independently and unidirectionally ventilated. Intrapulmonary chemoreceptor activity was altered by changing the PCO2 of the ventilatory gas (PICO2) to the vascularly isolated right lung (VIL); systemic chemoreceptor activity was altered by changing the PICO2 to the denervated left gas exchange lung (GEL). Respiratory amplitude and frequency responses to changes in intrapulmonary PCO2 were determined at four levels of systemic arterial PCO2 (PaCO2). The results indicate that elevating PaCO2 shifts the pulmonary CO2-response curves for both RA and f to the left and increases the sensitivity of the RA-CO2 response curve but decreases the sensitivity of the f-CO2 response curve. We conclude that (1) interaction occurs between intrapulmonary and systemic afferent activity in the generation of RA and f, (2) the nature of the interaction is synergism with respect to RA and interference with respect to f, and (3) the interaction is greater during hypocapnia than hypercapnia.

Animals↗

PubMed1983

The effect on breathing of abruptly reducing the discharge of central chemoreceptors.

Tris, a powerful CO2 buffer, was injected through one vertebral artery directly at the central chemoreceptive region in bilaterally vagotomized pentobarbitone anaesthetized cats. This was intended to reduce central chemoreceptor drive abruptly. Injections in inspiration shortened that inspiration and prolonged the following expiration. Injections given early in expiration often prolonged that expiration and also the following inspiration, but most injections given in an expiration shortened that expiration and also shortened the following inspiration. Tidal volume (VT) was invariably reduced. A plot of VT against delay from an injection to the termination of inspiration shows that VT falls with a half time of about one second. The changes in the pattern of breathing were similar to those after abrupt removal of carotid body chemoreceptor discharge (Nye et al., 1981) though the latency to the first response of air flow was about 100 msec longer. These observations support the idea that peripheral and central chemoreceptors have similar connections with the respiratory centre.

Animals↗

PubMed1986

Stimulation of respiratory changes in alae nasi length by chemoreceptor activation.

Respiratory-related changes in length of the nasal dilator muscle, the alae nasi muscle, were measured using sonomicrometry in ten anesthetized (pentobarbital), tracheostomized, spontaneously breathing dogs. Piezoelectric crystals were inserted 7-25 mm apart along the direction of the alae nasi muscle fibers, and the effects of progressive hyperoxic hypercapnia and a peripheral and central chemoreceptor stimulant, nicotine (10-500 micrograms intravenously), were ascertained. The alae nasi shortened during inspiration in all animals, started to lengthen again towards the end of inspiration, returned to resting length during the first portion of expiration (Te-1), and remained at resting length for the remainder of expiration (Te-2). The amount of alae nasi inspiratory shortening was increased by occluding the airway for a single breath. Progressive hypercapnia caused progressive increases in the amount and velocity of nasal muscle inspiratory shortening during both unoccluded and occluded breaths; similar stimulatory effects on inspiratory shortening were seen following nicotine administration. Furthermore, both chemoreceptor stimulants caused a delay in the return of the muscle to its resting length during expiration, resulting in a significant increase in Te-1 relative to Te (Te-1/Te), and a greater amount of nasal muscle shortening to be present during Te-1. In some animals these agents also caused tonic shortening of the alae nasi, so that the muscle never returned to its resting length. These results suggest that inspiratory shortening of the alae nasi is inhibited by vagal inputs, but that chemoreceptor activation increases the amount of muscle shortening during both inspiration and early expiration.

Animals↗