Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Chemoreceptor”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 127 records · Page 7Linked to original sources
PubMed1999

Inhibition of baroreflex vagal bradycardia by selective stimulation of arterial chemoreceptors in rats.

We reported recently that hypoxia inhibits baroreflex vagal bradycardia (BVB) in rats and that this inhibition persists following chemoreceptor denervation. However, since it is possible that hypoxia also affects the central processing of chemoreceptive input, the existence of chemoreceptor-mediated inhibition of BVB cannot be ruled out. Therefore, we have studied whether selective chemoreceptor activation affects BVB in normoxic conditions. In pentobarbital-urethane-anaesthetized, succinylcholine-immobilized, artificially ventilated rats, BVB was provoked by electrical stimulation of the aortic depressor nerve. Arterial chemoreceptors were selectively activated by intracarotid injection of a minute amount of sodium cyanide. Cyanide injection consistently increased blood pressure while changing heart rate variably. BVB was inhibited in a dose-dependent manner. This inhibition, as well as changes in blood pressure and heart rate, was abolished following transection of the carotid sinus nerve (CSN) ipsilateral to the injection. Spinal cord transection at the C2 level did not affect the inhibition. On the other hand, intracarotid cyanide had no effect on bradycardia elicited by electrical stimulation of a peripheral cut end of the cervical vagus nerve. We conclude that chemoreceptor activation definitely inhibits BVB and that this inhibition is mediated by the CSN, and predominantly occurs in the central nervous system. The possibility is suggested that severe hypoxia suppresses not only BVB but also the chemoreceptor-mediated inhibition of BVB, both via the direct, central action.

Afferent Pathways↗
PubMed2000

Viral gene transfer of dominant-negative Kv4 construct suppresses an O2-sensitive K+ current in chemoreceptor cells.

Hypoxia initiates the neurosecretory response of the carotid body (CB) by inhibiting one or more potassium channels in the chemoreceptor cells. Oxygen-sensitive K(+) channels were first described in rabbit CB chemoreceptor cells, in which a transient outward K(+) current was reported to be reversibly inhibited by hypoxia. Although progress has been made to characterize this current with electrophysiological and pharmacological tools, no attempts have been made to identify which Kv channel proteins are expressed in rabbit CB chemoreceptor cells and to determine their contribution to the native O(2)-sensitive K(+) current. To probe the molecular identity of this current, we have used dominant-negative constructs to block the expression of functional Kv channels of the Shaker (Kv1.xDN) or the Shal (Kv4.xDN) subfamilies, because members of these two subfamilies contribute to the transient outward K(+) currents in other preparations. Delivery of the constructs into chemoreceptor cells has been achieved with adenoviruses that enabled ecdysone-inducible expression of the dominant-negative constructs and reporter genes in polycistronic vectors. In voltage-clamp experiments, we found that, whereas adenoviral infections of chemoreceptor cells with Kv1.xDN did not modify the O(2)-sensitive K(+) current, infections with Kv4.xDN suppressed the transient outward current in a time-dependent manner, significantly depolarized the cells, and abolished the depolarization induced by hypoxia. Our work demonstrate that genes of the Shal K(+) channels underlie the transient outward, O(2)-sensitive, K(+) current of rabbit CB chemoreceptor cells and that this current contributes to the cell depolarization in response to low pO(2).

Adenoviridae↗
PubMed1976

A pharmacological analysis of neurally induced inhibition of carotid body chemoreceptor activity in cats.

Experiments were performed to determine the mechanism by which centrifugal impulses in the carotid sinus nerve (CSN) reduce the frequency of impulse traffic in afferent chemoreceptor fibers from the carotid body in cats. Recordings of chemoreceptor activity were made from single- or few-fiber preparations dissected off the CSN, while the remainder of the CSN was stimulated electrically to produce neurally induced inhibition of chemoreceptor activity. Various drugs were injected either intravenously or directly into the arterial blood supply to the carotid body. We found that catecholamines (dopamine, norepinephrine and epinephrine) inhibited spontaneous chemoreceptor activity, and that alpha adrenergic antagonists abolished both this inhibition and that produced by electrical stimulation of the CSN in the same preparation. Atropine, but not nicotinic antagonists of acetylcholine, consistently blocked neurally induced inhibition but not that produced by catecholamines. Muscarinic agonists had no effect on spontaneous chemoreceptor activity. We conclude that centrifugal activity in the CSN causes release of endogenous catecholamines in the carotid body, and that these catecholamines mediate neurally induced inhibition of chemoreceptor activity is due to the vasomotor effects of acetylcholine.

Acetylcholine↗
PubMed1982

Chloral hydrate and the carbon dioxide chemoreceptor response: a study of puppies and infants.

CO2 chemoreceptor function was assessed during natural sleep and following the administration of 100 mg/kg of chloral hydrate to 26 puppies. With chloral hydrate-induced sleep, there were no significant changes in ventilation or in CO2 chemoreceptor response. The ventilation and CO2 chemoreceptor response of a group of infants in natural sleep were compared with those of a group receiving 50 mg/kg of chloral hydrate. Tidal volume O2 consumption, and CO2 elimination were slightly higher in the group given chloral hydrate. There was no difference in the CO2 chemoreceptor response. The proportion of time spent in rapid eye movement (REM) and non-rapid eye movement (NREM) sleep in chloral hydrate-induced sleep was similar to that occurring in natural sleep. Use of chloral hydrate stabilizes O2 consumption sleep. Use of chloral hydrate stabilizes O2 consumption and CO2 production, and it greatly facilitates the assessment of chemoreceptor function in infants. The CO2 chemoreceptor response appears not to be altered in puppies or infants.

Animals↗
PubMed1993

Modification of carotid chemoreceptor-induced changes in renal haemodynamics and function by carotid baroreflex in dogs.

1. Mongrel dogs were anaesthetized with thiopental sodium and chloralose and artificially ventilated. The carotid sinus regions were vascularly isolated and perfused either with arterial or mixed (arterial and venous) blood (PO2, 44.2 +/- 3.3 mmHg, mean +/- S.E.M.) to stimulate the chemoreceptors. Cervical vagosympathetic trunks were ligated and atenolol (2 mg kg-1, I.V.) was given in all dogs and gallamine triethiodide (3 mg kg-1 h-1, I.V.) was given in two dogs. Renal blood flow was measured by an electromagnetic flowmeter, glomerular filtration rate by creatinine clearance, sodium excretion by flame photometry and solute excretion by osmometry. The viability of the preparations was tested by recording total vascular capacitance responses to stimulation of carotid baro- and chemoreceptors. 2. In eleven tests in seven dogs at a constant aortic pressure of 88.9 +/- 2.6 mmHg stimulation of carotid chemoreceptors at a high carotid sinus pressure (194.0 +/- 3.6 mmHg) resulted in significant increases in urine flow of 22.8 +/- 3.0%, urinary sodium excretion of 30.7 +/- 5.2%, fractional sodium excretion of 35.3 +/- 18.6%, osmolar excretion of 17.5 +/- 4.1% and a decrease in free water clearance of 30.8 +/- 3.1% without significant changes in urinary sodium concentration, renal blood flow, glomerular filtration rate, and filtration fraction. 3. In seventeen tests in these seven dogs at a constant aortic pressure of 94.0 +/- 2.2 mmHg, stimulation of carotid chemoreceptor at a low carotid sinus pressure (72.0 +/- 1.3 mmHg) resulted in significant decreases in renal blood flow of 10.6 +/- 2.5%, glomerular filtration rate of 19.6 +/- 6.8%, filtration fraction of 13.2 +/- 5.5%, urine flow of 23.4 +/- 4.1%, urinary sodium concentration of 20.3 +/- 4.1%, urinary sodium excretion of 38.5 +/- 4.6%, fractional sodium excretion of 20.2 +/- 7.7%, osmolar excretion of 23.9 +/- 4.0% and an increase in free water clearance of 23.1 +/- 2.5%. 4. The results show that moderate stimulation of carotid chemoreceptors at a low carotid sinus pressure, when the activity in renal nerves is high and blood volume is low, can produce significant reflex decreases in renal haemodynamic and functional variables. However, at a high carotid sinus pressure when the renal sympathetic activity is low and blood volume is high, carotid chemoreceptor stimulation produces diuresis and natriuresis but no change in renal haemodynamics.

Animals↗
PubMed1977

Facilitation of Chemoreceptor-induced reflex vasoconstriction by intravertebral arterial administration of clonidine.

The influence of clonidine on the reflex vascular responses to stimulation of carotid body chemoreceptors and bilateral carotid occlusion was studied in morphine, chloralose-urethane anesthetized dogs. Bilateral carotid occlusion and intracarotid injection of nicotine (30 and 100 microgram) or sodium cyanide (200 and 500 microgram) elicited reflex vasoconstriction in the perfused gracilis muscle vascular bed. Infusion of clonidine (2-4 microgram/kg) into the vertebral artery significantly lowered blood pressure. Reflex vasoconstrictor responses to chemoreceptor stimulation were significantly enhanced after clonidine administration whereas reflex vasoconstrictor responses to carotid occlusion were markedly reduced. The facilitation of chemoreceptor reflex responses by clonidine was observed in dogs with intact or sectioned vagi and in animals in which the carotid arteries were perfused at constant blood flow. Inhibition of carotid occlusion responses by clonidine was observed in dogs with intact or sectioned vagi. Infusion of clonidine directly into the carotid arteries did not significantly alter responses to chemoreceptor stimulation. These experiments demonstrate that clonidine antagonizes the reflex vasoconstriction caused by carotid occlusion while potentiating the vasoconstriction elicited by chemoreceptor stimulation. The data suggest that clonidine exerts central actions which result in a facilitation of the chemoreceptor reflex and a simultaneously occuring hypotension which is probably due to an action on baroreceptor pathways.

Animals↗
PubMed1979

The effects of blood osmolality changes on cat carotid body chemoreceptors in vivo.

The possibility that carotid chemoreceptors respond to changes in plasma osmolality was investigated in the cat, perfusing the carotid artery with blood made hyper- or hypo-osmotic and recording chemoreceptor activity from carotid nerve fibers. Blood made hyperosmotic with sucrose or NaCl reduced the chemoreceptor discharge, while hypoosmotic blood increased chemoreceptor activity. The minimal osmolality variation necessary to obtain a detectable frequency change was 3--8% of the control. Frequency changes of 30% of the control were obtained with a 20% variation in osmolality. The frequency variations produced by the osmotic changes lasted as long as the infusion was maintained (up to 15 min). In some instances a rebound was observed when iso-osmotic saline was perfused again. A transient change in frequency and a clear rebound were obtained when blood made hypersomotic with glycerol was perfused. These effects probably reflect a rapid change in intracellular osmolality due to the free passage of glycerol across cellular membranes. The modifications in chemoreceptor activity consecutive to osmolality variations are the opposite of those observed in isolated and superfused carotid bodies. As it is known that osmolality values affect the smooth muscle of the blood vessels, we conclude that our results are mainly produced by changes in carotid body blood flow due to a direct effect of hyper- and hypo-osmotic solutions on vascular muscle tone. Chemoreceptor excitation during a decrease in blood osmolality may contribute reflexly to the increased vascular resistance observed during acute osmolality reductions in man.

Animals↗
PubMed1980

Baroreceptor and chemoreceptor reflexes in postganglionic neurones supplying skeletal muscle and hairy skin.

Postganglionic neurons supplying skeletal muscle and hairy skin of the cat's hindlimb were investigated for their reactions to stimulation of carotid baroreceptors and chemoreceptors in chloralose-anaesthetized, immobilized and artificially ventilated animals. The baroreceptors were stimulated by the pulsatile blood pressure and by pressure increases applied to an isolated carotid sinus (carotid blind sac) leaving only one intact buffer nerve. Chemoreceptors were stimulated by systemic hypoxia and by intracarotid bolus injections of CO2-saturated saline. The cardiac rhythmicity of activity in the postganglionic neurones (evaluated from the post-R-wave histograms) and the neurone reactions to intracarotid pressure increases were fairly well correlated, with a coefficient of r = 0.84. The time course and magnitude of inhibitory responses to intracarotid pressure increases were identical in some of the cutaneous postganglionic neurones and postganglionic neurones supplying skeletal muscle. The majority of the postganglionic neurones supplying skin, however, exhibited a weaker inhibitory response and a different time course in their activity during and after the sinus pressure increases. Muscle postganglionic neurones were excited and the majority of the cutaneous postganglionic neurones were inhibited by stimulations of arterial chemoreceptors produced by systemic hypoxia and by intracarotid injection of CO2-saturated saline. Small fractions of the post-ganglionic neurones supplying skin were excited by stimulation of arterial chemoreceptors. The activity of these cutaneous postganglionic neurones showed a strong cardiac rhythmicity. It is proposed that those postganglionic neurones supplying skin which are affected by stimulation of baro- and chemoreceptors in the same manner as are the postganglionic neurones supplying skeletal muscle may innervate cutaneous resistance (nutritional) vessels. It is likewise suggested that those cutaneous postganglionic neurones inhibited by stimulation of arterial chemoreceptors and under weak control by the arterial baroreceptors may innervate cutaneous capacitance and shunt vessels.

Animals↗
PubMed1999

Sensitivity of the mosquito Aedes aegypti (Culicidae) labral apical chemoreceptors to phagostimulants.

The feeding of Aedes aegypti (L.) on blood and nectar is induced by phagostimulants: adenine nucleotides and sugars respectively. This work examines the responses of the four chemoreceptor cells in the labral apical sensilla to these phagostimulants. The apical chemoreceptors can detect the presence of adenine nucleotides. This part of the response is in good agreement with the gorging behavior. The output of the chemoreceptors cannot distinguish among different adenine nucleotides or among their concentrations (0.01-1 mmol/l), whereas gorging behavior is affected by the identity of adenine nucleotides and by their concentrations. Hence the gorging behavior cannot be driven by the output of these chemoreceptors alone. To the presence of adenine nucleotides Cell 2 was the only cell that responded with high frequencies, while the response of Cell 4 was almost abolished. The response of Cell 2 to ATP depended on the mosquito's physiological state. This dependence accorded well with the gorging behavior; Cell 2 responded with a higher frequency to ATP in the gorging state, than when not in a gorging state. The responses to sucrose and fructose constituted the only case recorded in which all these chemoreceptors failed to respond. This depression of response implies that other chemoreceptors must be present as sugar detectors.

Journal Article↗
PubMed2000

Isoflurane does not depress the hypoxic response of rabbit carotid body chemoreceptors.

UNLABELLED: Whether volatile anesthetics have an effect on the peripheral chemoreceptors is controversial, possibly because of differences in end-tidal CO(2) concentrations. We studied the effect of isoflurane on the hypoxic chemosensitivity of carotid body chemoreceptors at three different PaCO(2) levels before and during the administration of 1.0% isoflurane (0.5 minimum alveolar anesthetic concentration) in six normothermic New Zealand white rabbits anesthetized with thiopental. The response of the chemoreceptors was fitted to the equation: Frequency (Hz) = a + b x PaCO(2) + c x (1/PaO(2)) + Dx (1/PaO(2))(2). Mean values for the coefficients a, b, c and d for the control state were -4.5, 0.13, 771, and 6332, respectively. This relationship was not changed by addition of isoflurane at 1.0% end-tidal concentration (P = 0.40, analysis of variance). We conclude that isoflurane at 1.0% end-tidal concentration does not depress the hypoxic response of rabbit carotid body chemoreceptors during either hypo-, normo-, or hypercapnia. IMPLICATIONS: By measuring single-fiber chemoreceptor activity in anesthetized rabbits, we showed that isoflurane at 1.0% end-tidal concentration does not depress the hypoxic chemosensitivity of peripheral chemoreceptors during either hypo-, normo-, or hypercapnia in this species.

Action Potentials↗
PubMed2001

Basic FGF localization in rat carotid body: paracrine role in O2 -chemoreceptor survival.

Exposure of perinatal rat carotid body (CB) O2-chemoreceptors to basic fibroblast growth factor (bFGF) or hypoxia in vitro increases mitotic activity. Using double-label immunofluorescence, we localized bFGF and its receptor (FGFR) to tyrosine hydroxylase-positive (TH+) chemoreceptors in vitro; bFGF immunoreactivity also localized to chemoreceptors in CB tissue sections. Mitotic activity, measured as percentage TH+ cells that took up bromodeoxyuridine, was relatively constant ( approximately 29%) in normoxic (20% O2) cultures grown with or without bFGF neutralizing antibody (nAb). However, the number of surviving chemoreceptors was significantly reduced in nAb-treated cultures. Under chronic hypoxia (6% O2), the presence of nAb significantly reduced chemoreceptor survival to approximately 70% of control, without affecting mitotic activity. Thus, autocrine/ paracrine actions of endogenous bFGF may help promote CB chemoreceptor survival.

Animals↗
PubMed1985

Peripheral chemoreceptors in respiratory oscillations.

The hypothesis that instability of cardiorespiratory control may depend on the response and sensitivity of carotid body chemoreceptors to arterial blood gases was studied in anesthetized cats under three different experimental conditions. 1) Following administration of the peripheral dopamine receptor blocker [domperidone (0.6-0.8 mg X kg-1, iv)], carotid chemoreceptor activity and its sensitivity to CO2 during hypoxia increased, leading to cardiorespiratory oscillations at low arterial PO2 in four of eight cats. Inhalation of 100% O2 promptly decreased chemoreceptor activity and eliminated the oscillations. Inhalation of CO2 stimulated the chemoreceptor activity and ventilation but did not eliminate the oscillations. Bilateral section of carotid sinus nerves abolished the cardiorespiratory oscillations. The implication is that the dopaminergic system in the carotid body keeps chemoreceptor responses to blood gas stimuli suppressed and hence cardiorespiratory oscillations damped. 2) Hypotension and circulatory delay induced by the partial occlusion of venous return led to cardiorespiratory oscillations at low but not at high arterial PO2. 3) A few cats developed cardiorespiratory oscillations without any particular experimental intervention. These oscillations were independent of arterial PO2 and chemoreceptor activity. Thus it is reasonable to conclude that the peripheral chemoreflex can play a critical role in developing cardiorespiratory oscillations in certain instances.

Animals↗
PubMed1984

Alpha-adrenergic-mediated reduction in coronary blood flow secondary to carotid chemoreceptor reflex activation in conscious dogs.

We examined the late coronary vascular response to carotid chemoreceptor reflex activation in normal, conscious dogs instrumented for the measurement of right main and left circumflex coronary artery blood flows, arterial and right ventricular pressures, and arterial and coronary sinus blood gases and O2 contents. With heart rate held constant by electrical stimulation, and with respiration controlled or allowed to vary spontaneously, carotid chemoreceptor reflex activation (induced by intracarotid nicotine) elicited a striking biphasic coronary vascular response characterized by an early dilation (previously described) and a late constriction. For example, with respiration controlled and with the autonomic nervous system intact, carotid chemoreceptor reflex activation resulted in a late increase in arterial pressure (19 +/- 4%; P less than 0.002), absolute reductions in right main (24 +/- 4%; P less than 0.002), and left circumflex (12 +/- 2%; P less than 0.004) coronary blood flows, and increases in right (62 +/- 13%; P less than 0.002) and left (26 +/- 3%; P less than 0.0001) coronary resistances. This carotid chemoreceptor reflex activation-induced late coronary constriction was also associated with a concomitant increase in myocardial oxygen extraction, i.e., arterial oxygen content remained constant, while coronary sinus oxygen content decreased (19 +/- 6%; P less than 0.04). Neither propranolol nor atropine had any significant effect on the magnitude of the right coronary constriction. However, both the absolute reduction in right coronary blood flow and increase in right coronary resistance were abolished by phentolamine. Furthermore, either total cardiac denervation or adrenalectomy significantly attenuated (P less than 0.01) carotid chemoreceptor reflex activation-induced reductions in right coronary blood flow and increase in right coronary resistance. We conclude that, with autonomic nervous system activity intact, carotid chemoreceptor reflex activation can elicit an absolute reflexly mediated reduction in coronary blood flow in the normal, conscious dog, despite an increase in arterial pressure. The mechanism of this vasoconstriction involves alpha-adrenergic receptor stimulation mediated by both cardiac sympathetic nerves and circulating catecholamines.

Adrenalectomy↗
PubMed1980

The role of sympathetic nerves in the activation of the carotid body chemoreceptors at birth in the sheep.

Carotid body chemoreceptor afferent discharge was recorded in the sinus nerve of sheep fetuses within a few days of term, exteriorized from ewes given pentobarbitone anaesthesia, and in six newborn lambs, 7-21 h old. Chemoreceptor discharge, defined as such since it was irregular, had no relation to the heart beat and was excited by hypoxia, hypercapnia, H+ and NaCN, was recorded in only 8 out of 20 fetuses. It was abundant in both the newborn lambs and also in fetus carotid bodies studied in vitro. Although electrical stimulation of the sympathetic fibres to the carotid body excited the fetal chemoreceptors and caused a fall in carotid body blood flow, the fetal chemoreceptors still responded to natural stimuli and drugs in both fetus and lamb after the sympathetic pathway had been cut. Further, there appeared to be clear dissociation of chemoreceptor and sympathetic activation shortly after birth. These results confirm and extend earlier studies and they suggest that, although the sympathetic pathway may contribute to chemoreceptor activation at birth, other, possibly more important, factors must be involved. These are discussed.

Action Potentials↗
PubMed1983

Reflex activation of postganglionic vasoconstrictor neurones supplying skeletal muscle by stimulation of arterial chemoreceptors via non-nicotinic synaptic mechanisms in sympathetic ganglia.

Postganglionic sympathetic neurones supplying skeletal muscle and skin can be activated from the preganglionic site via cholinergic nicotinic, muscarinic and noncholinergic synaptic mechanisms. The experiments described in this paper were designed in order to show that postganglionic vasoconstrictor neurones supplying skeletal muscle can be activated by the naturally occurring discharge pattern in preganglionic axons when the nicotinic transmission is blocked. For this purpose, the activity was recorded simultaneously from postganglionic vasoconstrictor axons supplying skeletal muscle and vasoconstrictor axons supplying hairy skin. The preganglionic neurones were driven reflexly by stimulation of the arterial chemoreceptors. 1) During blockade of nicotinic transmission muscle vasoconstrictor neurones were activated via the CNS during stimulation of arterial chemoreceptors. This activation is either generated by muscarinic action of released acetylcholine or by a noncholinergic synaptic mechanism. 2) Postganglionic cutaneous vasoconstrictor neurones were inhibited during stimulation of arterial chemoreceptors. During blockade of cholinergic nicotinic transmission these neurones were not activated reflexly by stimulation of arterial chemoreceptors although they received inputs via cholinergic muscarinic and noncholinergic synaptic mechanisms. 3) The results illustrate that postganglionic vasoconstrictor neurones supplying skeletal muscle can not only be activated via non-nicotinic synaptic mechanisms through synchronous repetitive electrical stimulation of preganglionic axons but also by the discharge pattern produced in preganglionic neurones during stimulation of arterial chemoreceptors.

Animals↗
PubMed1988

Effects of changes in chemoreceptor activity on extracellular K+ and Ca2+ activities in the cat carotid body.

In anaesthetized, paralysed and artificially ventilated cats triple-barrelled ion-selective microelectrodes (ISMs) were inserted into the right carotid body in order to measure extracellular activities of K+ ([K+]o) and Ca2+ ([Ca2+]o) simultaneously. In 3 experiments a method involving iron deposition located the tips of the ISMs in the cellular islands of the organ. A thin cannula inserted into the right carotid artery (i.c.) via the lingual artery was used to infuse Ringer-Locke solutions (0.1-0.5 ml/min) containing either sodium cyanide (NaCN), acetylcholine (ACh) or dopamine (DA). Analysis of the effects of administration of NaCN (20-100 micrograms/min i.c.) showed that during this procedure [K+]o increased and [Ca2+]o decreased by mean values (+/- S.D.) of 0.99 +/- 0.82 and 0.22 +/- 0.06 mM respectively. During administration of ACh (20-50 micrograms/min i.c.) [K+]o increased and [Ca2+]o decreased respectively by mean values (+/- S.D.) of 3.18 +/- 3.0 and 0.31 +/- 0.14 mM. Decreases in [K+]o and [Ca2+]o by mean values (+/- S.D.) of 1.53 +/- 1.64 and 0.34 +/- 0.33 mM respectively were associated with administration of DA (20-50 micrograms/min i.c.). The predominant influences exerted by NaCN and ACh on chemoreceptor activity were excitatory whereas administration of DA caused either inhibition, excitation or a combination of these two effects. Stimulation of the sympathetic supply to the carotid body was associated with either increases, decreases or no reaction of chemosensory activity, [K+]o and [Ca2+]o. The changes in [K+]o associated with the various procedures may reflect the state of polarization within the chemoreceptor complex. Decreases in [Ca2+]o usually accompanied the performance of all procedures and may have resulted from an increased influx of this ion from the interstitial fluids into the cells for the purpose of provoking neurotransmitter release. However, the time course of the changes in [K+]o and [Ca2+]o were considerably slower in onset and recovery than the associated alterations in chemoreceptor activity. Therefore, it is unlikely that these ion changes are directly related to chemoreception but rather represent recovery processes after chemoreceptor modulation. It should be noted that the response times of the ISMs used in this study were too slow to register any rapid changes in [K+]o or [Ca2+]o associated with altered chemoreceptor activity.

Acetylcholine↗
PubMed1979

Reflex stimulation of aortic chemoreceptors and the role of vascular receptors.

Impulses were recorded in single afferent fibres of aortic chemoreceptors of cats anaesthetized with chloralose. As expected raising the blood pressure (BP) passively by occluding the abdominal aorta, consistently reduced or abolished the activity of the chemoreceptors. This reduction persisted for as long as the BP remained high. Stimulating the sensory receptors of the small intestines increased the activity of 10 aortic chemoreceptors. The increased activity persisted after bilateral adrenalectomy but it was abolished by blocking the nerves of the mesentery with xylocaine. The increased activity was noteworthy because it occurred in spite of the rise in blood pressure (that always occurred when the intestines were squeezed) which by itself would tend to reduce the activity of the chemoreceptors. It was concluded that stimulating the intestinal receptors produces a reflex increase in the activity of aortic chemoreceptors by causing a reduction of glomeral blood flow through impulses in the sympathetic fibres.

Adrenal Glands↗
PubMed1988

Peripheral chemoreceptor CO2 response during hyperoxia in the 14-day-old awake lamb.

We studied the interaction of O2 and CO2 at the peripheral chemoreceptors in 6 two-week-old awake lambs. The method used, which selectively tested the peripheral chemoreceptors, measured the immediate ventilatory (VE) response to pure O2 and then to O2 + CO2. From room air, the animal was switched abruptly to either pure O2 or O2 + 5% CO2, O2 + 7.5% CO2, or O2 + 10% CO2. VE was measured before and 8-10 sec after a step change in the inspired gas. In response to pure O2, VE/kg dropped 131 +/- 30 ml/min.kg (38%). Repeat O2 tests performed with the addition of CO2 showed that CO2 interacted to blunt the response to pure O2; the VE change from pre-test baseline to 8-10 sec being -77 +/- 42, -18 +/- 25, and +8.5 +/- 60 for 5%, 7.5%, and 10% added CO2 respectively. Carotid body denervation eliminated the immediate VE responses to O2 and CO2. We conclude that in the 2-week-old awake lamb, (1) hyperoxia suppresses the O2 drive output of the peripheral chemoreceptors, (2) during hyperoxia O2 and CO2 still interact at the chemoreceptor level, and (3) despite hyperoxia, the peripheral chemoreceptors retain a substantial graded response to incremental transient CO2 challenge.

Animals↗