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 91 records · Page 5Linked to original sources
PubMed2006

Cardiac sympathetic afferent stimulation augments the arterial chemoreceptor reflex in anesthetized rats.

Chronic heart failure (CHF) is well known to be associated with both an enhanced chemoreceptor reflex and an augmented cardiac "sympathetic afferent reflex" (CSAR). The augmentation of the CSAR may play an important role in the enhanced chemoreceptor reflex in the CHF state because the same central areas are involved in the sympathetic outputs of both reflexes. We determined whether chemical and electrical stimulation of the CSAR augments chemoreceptor reflex function in normal rats. Under anesthesia, renal sympathetic nerve activity (RSNA) and mean arterial pressure (MAP) were recorded. The chemoreceptor reflex was tested by unilateral intra-carotid artery bolus injection of potassium cyanide (KCN) and nicotine. We found that 1) left ventricular epicardial application of capsaicin increased the pressor responses and the RSNA responses to chemoreflex activation induced by both KCN and nicotine; 2) when the central end of the left cardiac sympathetic nerve was electrically stimulated, both the pressor and the RSNA responses to chemoreflex activation induced by KCN were increased; 3) pretreatment with intracerebroventricular injection of losartan (500 nmol) completely prevented the enhanced chemoreceptor reflex induced by electrical stimulation of the cardiac sympathetic nerve; and 4) bilateral microinjection of losartan (250 pmol) into the nucleus tractus solitarii (NTS) completely abolished the enhanced chemoreceptor reflex by epicardial application of capsaicin. These results suggest that both the chemical and electrical stimulation of the CSAR augments chemoreceptor reflex and that central ANG II, specially located in the NTS, plays a major role in these reflex interactions.

Analgesics, Non-Narcotic↗
PubMed1999

Developmental changes in membrane properties of chemoreceptor afferent neurons of the rat petrosal ganglia.

Carotid body chemoreceptors increase their responsiveness to hypoxia in the postnatal period, but the mechanism for this increase is unresolved. The purpose of the present study was to examine developmental changes in cellular characteristics of chemoreceptor afferent neurons in the petrosal ganglia with the underlying hypothesis that developmental changes occur and may account for the developmental increase in chemoreceptor responsiveness. Chemoreceptor complexes (carotid body, sinus nerve, glossopharyngeal nerve, and petrosal ganglia) were harvested from rats, aged 3-40 days, and intracellular recordings were obtained from petrosal ganglion neurons using sharp electrode impalement. All chemoreceptor neurons across ages were C fibers with conduction velocities <1 m/s and generated repetitive action potentials with depolarization. Resting membrane potential was -61.3 +/- 0.9 (SE) mV (n = 78) and input resistance was 108 +/- 6 MOmega and did not significantly change with age. Cell capacitance was 32.4 +/- 1.7 pF and did not change with age. Rheobase averaged 0.21 +/- 0.02 nA and slightly increased with age. Action potentials were followed by an afterhyperpolarization of 12.4 +/- 0.6 mV and time constant 6.9 +/- 0.5 ms; only the time constant decreased with age. These results, obtained in rat, demonstrate electrophysiologic characteristics which differ substantially from that previously described in cat chemoreceptor neurons. In general developmental changes in cell characteristics are small and are unlikely to account for the developmental increase in chemoreceptor responsiveness with age.

Action Potentials↗
PubMed1978

Depression of ventilation by dopamine in man. Evidence for an effect on the chemoreceptor reflex.

Dopamine is present in the carotid body and has been postulated to be an inhibitory neurotransmitter. The purpose of this study was to determine the effects of dopamine on ventilation in man and to examine its mechanism of action. Dopamine (0.5-10 mug/kg per min) was infused in eight normal men at different levels of arterial chemoreceptor activity, produced by varying the inspired Po(2). During normoxia dopamine produced a small decrease in minute ventilation (Ve) and an increase in arterial Pco(2). When arterial chemoreceptors were stimulated by hypoxia, infusion of dopamine produced a marked initial depression of Ve followed by a sustained although less pronounced decrease in Ve. An increase in Pa(co) (2) and a decrease in Pao(2) were also observed. When arterial chemoreceptor activity was suppressed by hyperoxia, infusion of dopamine did not affect ventilation. Subjects also breathed a hypercarbic, hyperoxic gas mixture. The hypercarbia produces hyperventilation by stimulating central chemoreceptors, whereas the hyperoxia suppresses peripheral chemoreceptors. Dopamine did not alter ventilation while the subjects were breathing this gas mixture. These studies suggest that dopamine suppresses ventilation in man through an action on the arterial chemoreceptor reflex. These findings support the hypothesis that dopamine is an inhibitory neurotransmitter in the carotid body, and that release of dopamine may modulate the sensitivity of peripheral arterial chemoreceptors.

Adult↗
PubMed2002

Influence of the stimulation of carotid body chemoreceptors on the gastric mucosal blood flow in artificially ventilated and spontaneously breathing rats.

The cardiovascular effects of the stimulation of arterial chemoreceptors are different in spontaneously breathing and artificially ventilated animals. Respiratory failure and long term sojourn at high altitude coincide frequently with the occurrence of gastric ulceration. In both these situations a profound stimulation of arterial chemoreceptors is present. The purpose of the paper was to investigate the reflex effect of stimulation carotid chemoreceptors on gastric mucosal blood flow in the rat. Arterial chemoreceptors were stimulated by two methods (I) substitution gas mixture of 10% oxygen in nitrogen for room air and (II) direct injection of acid saline ( 0.05 ml, pH = 6.8) into the distal part of left common carotid artery. In artificially ventilated rats stimulation of arterial chemoreceptors caused significant increase in gastric mucosal vascular resistance, accompanied by marked decline in blood flow. This effect was mediated by adrenergic mechanism. On the contrary to artificially ventilated rats, decline of gastric mucosal vascular resistance with concomitant increase in blood flow was found in spontaneously breathing animals. This effect was not abolished either by phentolamine or atropine. As vasodilatatory effect of arterial chemoreceptors stimulation was abolished by bilateral vagotomy, we postulate that non adrenergic and non cholinergic vagal fibers mediate observed vascular changes in gastric mucosa in spontaneously breathing rats. We hypothesize that in artificially ventilated patients with respiratory failure stimulation of arterial chemoreceptors by hypoxemia and or acidosis may contribute to the development of gastric mucosal lesions.

Acids↗
PubMed1975

Relationship between carotid chemoreceptor activity and ventilation in the cat.

The steady-state stimulus-response relations between arterial P02 and PCO2 and the mean activity of carotid chemoreceptors (single and multi-fiber) and ventilation were simultaneously recorded in 48 anesthetized cats. The carotid chemoreceptor activity varied linearly with the increase of arterial PCO2, below and above the normal value, at any given level of arterial P02. A decrease in arterial P02 increased the activity of the carotid chemoreceptors and increased its sensitivity to changes in arterial PCO2, showing multiplicative stimulus interaction. The authors also found that the response in ventilation during hypoxia to changes in arterial PCO2 below the normal value was smaller than that to changes above it, unlike the response of carotid chemoreceptors. This arterial PCO2 quasi-threshold for ventilation was, therefore, not due to a corresponding threshold for the activity of the carotid chemoreceptors but to a central mechanism. Above the central PaCO2 threshold, the ventilatory response to changes in PaCO2 and Pa02 resembled that of chemoreceptors but the ventilation dependent on hypoxia was greater than that could be directly accounted for by the activity of peripheral chemorecepors. A multiplicative interaction between the activity of peripheral chemoreceptors and central CO2 excitation appears to play a role in the regulation of ventilation.

Animals↗
PubMed1986

Influence of ganglioglomerular nerve on carotid chemoreceptor activity in the cat.

The dependence of the carotid chemoreceptor responses to blood-borne stimuli on the ganglioglomerular nerve (GGN) activity was investigated in cats which were anesthetized, paralyzed and artificially ventilated. The activity of a few carotid chemoreceptor afferents from a slip or from the cut left carotid sinus nerve (CSN) and the activity of a few GGN fibers were recorded. The responses of the same chemoreceptor afferents to steady-state hypoxia at a constant paCO2 and to steady-state hypercapnia during hyperoxia were compared before and after the transection of the ipsilateral ganglioglomerular nerve (IGGN). Similarly the effects of IGGN transection on the responses of the same chemoreceptor afferents to graded doses of intravenous injections of sodium cyanide (20-60 micrograms) and nicotine (20-60 micrograms) at constant blood gas levels were studied. On the average, IGGN transection during normoxia only slightly changed the carotid chemoreceptor activity. Also, it did not significantly change the hypoxic and hypercapnic responses, and those to sodium cyanide and nicotine injections. Thus, the mean carotid chemoreceptor responses to physiological and pharmacological stimuli were largely independent of the GGN. However, certain GGN fibers were strongly stimulated by hypoxia and hypercapnia. Clearly, the total GGN traffic to the carotid body was not sufficiently strong to exert a significant control over the mean carotid chemoreceptor activity.

Animals↗
PubMed1972

The role of the solitary and paramedian reticular nuclei in mediating cardiovascular reflex responses from carotid baro- and chemoreceptors.

1. With dye-filled micro-electrodes single neurones in the medulla of anaesthetized paralysed cats were identified which: (a) fired rhythmically in synchrony with or were modulated by the cardiac cycle, and which ceased firing with occlusion of the ipsilateral common carotid artery (carotid sinus baroreceptor neurones); (b) were excited by stimulation of carotid body chemoreceptors by close intra-arterial injection of lobeline into the thyroid artery (carotid body chemoreceptor neurones).2. Twelve carotid baroreceptor neurones were identified, in thirty-three cats, nine of which were localized in the intermediate area of the nucleus of the solitary tract (NTS) within 1 mm ahead of or behind the obex; three units were located either in the parahypoglossal area or the dorsal portion of the paramedian reticular nucleus (PRN).3. Of the twenty-one carotid chemoreceptor neurones which were identified, thirteen were localized in the NTS, three in the parahypoglossal area and four in the dorsal PRN.4. Bilateral lesions of the paramedian reticular area of medulla destroying the PRN, abolished or reversed the depressor response to electrical stimulation of myelinated fibres of the carotid sinus nerve (CSN), attenuated the depressor response to carotid sinus stretch and augmented the pressor response to chemoreceptor stimulation by lobeline. Such lesions did not significantly alter the reflex heart rate responses.5. Small lesions of the NTS within an area 1 mm rostral to the obex abolished all reflex blood pressure and heart rate responses to electrical stimulation of the CSN or natural stimulation of carotid baro- or chemoreceptors.6. Baroreceptors and chemoreceptors of the CSN project both to the intermediate zone of the NTS and to more medial areas of the medulla, particularly the dorsal PRN and parahypoglossal area.7. The PRN serves to mediate the reflex depressor, but not cardio-vagal, response from myelinated baroreceptors and buffers the pressor responses from chemoreceptors; it may serve as an important area integrating cardiovascular activity descending from forebrain, brain stem and cerebellum with baroreceptor reflexes.8. Cardiovascular reflex responses arising from non-myelinated baroreceptors and all chemoreceptors are mediated by neurones in the intermediate area of the NTS.

Animals↗
PubMed1977

The carotid chemoreceptor input to the respiratory neurones of the nucleus of tractus solitarus.

1. An investigation has been made into the connexions between the carotid body chemoreceptors and the dorsal respiratory neurones of the cat's medulla.2. In confirmation of previous work these neurones were found to be all inspiratory in firing pattern and to fall into two categories, Ralpha (forty-four units) which fire only with the central inspiratory rhythm and Rbeta (thirty-two neurones) that are also excited by lung inflation. Both categories were shown to be excited by stimuli delivered to the carotid bodies during inspiration but, with a single exception, not during expiration.3. When Rbeta neurones were made to fire tonically in expiration by maintained lung inflation, chemoreceptor activation inhibited this discharge in 7/11 cases, the remainder being unaffected.4. Iontophoretically applied DL-homocysteic acid or glutamate made both Ralpha and Rbeta neurones fire tonically in expiration. Chemoreceptor stimulation during expiration inhibited this activity in all neurones tested (nine Ralpha and three Rbeta cells).5. Using the measurement of the antidromic latency to spinal stimulation as an index of membrane potential, evidence was obtained that any subthreshold influence of the chemoreceptors on dorsal respiratory neurones during expiration was inhibitory (9/18 cases).6. It is concluded that chemoreceptors do not even subliminally excite dorsal inspiratory neurones during expiration; such influence as they have then is inhibitory. Possible reasons for this difference in chemoreceptor influence during inspiration and expiration are discussed. It is suggested that chemoreceptor excitation reaches them only as part of an enhanced central inspiratory drive from an as yet unknown source.

Action Potentials↗
PubMed1983

Effects of ouabain on carotid body chemoreceptor activity in the cat.

The effects of infusions of ouabain on chemoreceptor activity recorded from the peripheral end of a sectioned carotid sinus nerve were studied in cats anaesthetized with pentobarbitone. Ouabain caused a marked increase in chemoreceptor discharge followed by a decline in discharge to frequencies near or below the pre-ouabain level; during the latter period further administration of ouabain had no effect. Infusion of ouabain during hypoxia further increased the chemoreceptor discharge, but this effect was short-lasting. On intracarotid administration ouabain was less effective in cats with the ganglioglomerular (sympathetic) nerves cut, whereas on intravenous administration no significant difference was observed. Following intravenous administration of ouabain the chemoreceptor peak discharge occurred with dose levels similar to those needed to cause cardiac arrhythmias, but following intracarotid administration the chemoreceptor discharge peaked at doses about 40% of those causing arrhythmias. During ouabain-induced excitation the stimulatory action of NaCN, CO2-equilibrated Locke solution and acetylcholine was potentiated, as was the chemo-inhibition induced by dopamine. During the post-excitatory period the responses evoked by these substances were reduced or abolished. Neither mecamylamine, a nicotinic antagonist, nor physostigmine, an anti-cholinesterase, affected the response of the carotid chemoreceptors to ouabain. The major finding of this study was that ouabain initially 'sensitizes' the carotid body chemoreceptors and then 'desensitizes' them. The most likely mechanism responsible for these effects is the well established Na+--K+-ATPase-inhibiting property of ouabain.

Action Potentials↗
PubMed1977

Amino acid chemoreceptors of Bacillus subtilis.

Specificities of chemoreceptors for the 20 common amino acids, toward which Bacillus subtilis shows chemotaxis, were assessed by competition ("jamming") experiments using a modification of the traditional capillary assay, called the "sensitivity capillary assay." Many amino acids were sensed by at least two chemoreceptors. All the highest affinity chemoreceptors for the amino acids were distinct, except glutamate and aspartate, which may share one chemoreceptor, and tyrosine, for which the data could not be collected due to low solubility. The data suggest the hypothesis that each amino acid-chemoreceptor complex binds to a different signaler (from each amino acid-chemoreceptor complex binds to a different signaler (from which signals travel to the flagella to modify behavior appropriately), and that many of the signalers can also bind other attractant-chemoreceptor complexes as antagonists (no signals to flagella).

Amino Acids↗
PubMed2000

Polar clustering of the chemoreceptor complex in Escherichia coli occurs in the absence of complete CheA function.

Bacterial chemotaxis requires a phosphorelay system initiated by the interaction of a ligand with its chemoreceptor and culminating in a change in the directional bias of flagellar rotation. Chemoreceptor-CheA-CheW ternary complexes mediate transduction of the chemotactic signal. In vivo, these complexes cluster predominantly in large groups at the cell poles. The function of chemoreceptor clustering is currently unknown. To gain insight into the relationship between signaling and chemoreceptor clustering, we examined these properties in several Escherichia coli mutant strains that produce CheA variants altered in their ability to mediate chemotaxis, autophosphorylate, or bind ATP. We show here that polar clustering of chemoreceptor complexes does not require functional CheA protein, although maximal clustering occurred only in chemotactically competent cells. Surprisingly, in cells containing a minimum of 13 gold particles at the cell pole, a significant level of clustering was observed in the absence of CheA, demonstrating that CheA is not absolutely essential for chemoreceptor clustering. Nonchemotactic cells expressing only CheA(S), a C-terminal CheA deletion, or CheA bearing a mutation in the ATP-binding site mediated slightly less than maximal chemoreceptor clustering. Cells expressing only full-length CheA (CheA(L)) from either a chromosomal or a plasmid-encoded allele displayed a methyl-accepting chemotaxis protein localization pattern indistinguishable from that of strains carrying both CheA(L) and CheA(S), demonstrating that CheA(L) alone can mediate polar clustering.

Alleles↗
PubMed1976

Effect of stimulation of carotid chemoreceptors on total and regional cerebral blood flow.

This study was performed to determine whether stimulation of the carotid chemoreceptors increases total or regional cerebral blood flow and whether activation of arterial chemoreceptors contributes to cerebral vasodilation during systemic hypoxemia. In anesthetized and ventilated dogs, carotid chemoreceptors were stimulated with nicotine or hypoxic and hypercapnic blood. To measure total and regional cerebral blood flow, we used labeled 15-mu microspheres. Stimulation of chemoreceptors did not increase cerebral blood flow or produce significant redistribution of cerebral blood flow, even though the chemoreflex was intact in these animals (as manifested by vasoconstriction in muscle, kidney, and small bowel) and the cerebral vessels dilated in response to systemic hypercapnia. In other studies in anesthetized, ventilated dogs and rhesus monkeys, cerebral vasodilator responses to systemic hypoxemia were observed before and after denervation of carotid and aortic chemoreceptors. Systemic hypoxemia produced large and equivalent increases in cerebral blood flow before and after chemodenervation. We conclude that stimulation of carotid chemoreceptors does not produce cerebral vasodilation and that chemoreceptors do not contribute significantly to cerebral vasodilation during systemic hypoxemia.

Animals↗
PubMed1986

The role of the glycine sensitive area of the ventral medulla in cardiovascular responses to carotid chemoreceptor and peripheral nerve stimulation.

The present study on cats anaesthetised with Althesin, which unlike more commonly used anaesthetics does not prevent reflex activation of the brain-stem defence areas, reaffirmed that carotid chemoreceptor stimulation and radial nerve stimulation can evoke the visceral components of the alerting stage of the defence response (visceral alerting response). This includes tachycardia, mesenteric vasoconstriction but vasodilatation in skeletal muscle which is not secondary to the hyperventilation. However, mild chemoreceptor stimulation which evoked but a weak hyperventilation elicited bradycardia and vasoconstriction is mesentery and in muscle i.e. a response comparable with that evoked by chemoreceptor stimulation under chloralose or barbiturate anaesthesia. This suggests that chemoreceptor stimulation can evoke two separate patterns of response, the visceral alerting response predominating when the defence areas are strongly activated. The efferent pathway from the defence areas is known to synapse in the 'glycine sensitive area' of the ventral medulla which contains neurones whose activity seems to provide the main sympatho-excitatory drive for normal arterial pressure. Bilateral application of glycine to that area produces a pronounced fall in arterial pressure, apnoea and greatly attenuates the response to defence area stimulation, the vasoconstrictor components being abolished. In the present study bilaterally applied glycine abolished the muscle vasodilatation of the visceral alerting response evoked by chemoreceptor and radial nerve stimulation but both stimuli evoked vasoconstriction in mesenteric and muscle vasculature at least until arterial pressure was very low. It is proposed that both chemoreceptor and peripheral nerve stimulation can activate the defence areas to produce a visceral alerting response which is relayed via neurones of the glycine sensitive area.(ABSTRACT TRUNCATED AT 250 WORDS)

Afferent Pathways↗
PubMed1984

The afferent pathway for carotid body chemoreceptor input to the hypothalamic supraoptic nucleus in the rat.

The pathway for chemoreceptor input to hypothalamic supraoptic nuclei has been examined in anaesthetised lactating and non-lactating rats. In lactating rats, the increase in intramammary pressure following bilateral carotid occlusion, which is probably mainly due to vasopressin, was abolished by lesions in the septum, but not by lesions in more caudal regions of the hypothalamus. In non-lactating rats, electrophysiological experiments demonstrated that the input from carotid body chemoreceptors to phasically-discharging supraoptic neurones is ipsilateral only. The effects of chemoreceptor stimulation on the neurones can be mimicked by electrical stimulation within the medial preoptic area and anterior hypothalamus in a region medial and rostral to the supraoptic nuclei. Lesions within this region abolish the chemoreceptor input to the supraoptic nuclei, but leave the baroreceptor input intact. It is proposed that chemoreceptor afferents to the supraoptic nuclei pass in the lateral hypothalamus to the region of the septum where they turn medially and descent through the medial part of the rostral hypothalamus. The results are discussed in terms of the general role of the chemoreceptor reflex and, more specifically, with respect to the possible significance of vasopressin in the control of arterial blood pressure.

Afferent Pathways↗
PubMed2001

Chronic hypoxia enhances endothelin-1-induced intracellular calcium elevation in rat carotid body chemoreceptors and up-regulates ETA receptor expression.

Endothelin-1 (ET-1) excites carotid body (CB) chemoreceptors and induces mitosis of the chemoreceptors in chronic hypoxia. The aim of the present study was to examine the hypothesis that up-regulation of both ETA receptor and endogenous ET-1 expression in CB chemoreceptors enhances the response of intracellular Ca2+ to ET-1 following adaptation to chronic hypoxia (10% inspired O2 for 3-4 weeks). Cytosolic free [Ca2+] ([Ca2+]i) in type-I (glomus) cells freshly dissociated from rat CBs was measured by spectrofluorometry. Application of exogenous ET-1 (1-100 nM) concentration-dependently elevated [Ca2+]i in the glomus cells. This response to ET-1 (100 nM) was 49% greater in the chronically hypoxic (CH) group. The ET-1 response was abolished completely by the ETA receptor antagonist BQ610 (1 microM), but not by the ETB antagonist BQ788 (1 microM). The transient [Ca2+]i elevation induced by caffeine (30 mM) in the normoxic group was similar to that in the CH group, suggesting no differences in the intracellular Ca2+ stores. In situ hybridization with a digoxigenin-labelled antisense ETA receptor mRNA oligonucleotide probe revealed very intense and ubiquitous specific expression of ETA receptors in the lobules of glomus cells in the CH group, whereas staining in normoxic controls was light. Immunohistochemical studies revealed intense cytoplasmic staining for ET-1-immunoreactivity in most of the cell clusters in glomera in the CBs of CH rats but was faint in normoxic CBs. These findings indicate increased expression of both the ETA receptor and ET-1 in CB chemoreceptors during chronic hypoxia. Taken together, our results suggest that the [Ca2+]i response to ET-1 in rat CB chemoreceptors is augmented by up-regulation of ETA receptors and ET-1 expression. The enhancement of the paracrine/autocrine effect of ET-1 on the chemoreceptors is consistent with an excitatory and mitogenic role of the ET-1 and ETA receptor in the CB during chronic hypoxia.

Adaptation, Physiological↗
PubMed1988

Locations of medullary neurons with non-phasic discharges excited by stimulation of central and/or peripheral chemoreceptors and by activation of nociceptors in cat.

The activity of medullary neurons (146 units) with non-phasic discharges was recorded extracellularly in decerebrated, spontaneously breathing cats. The firing rate changes were studied during injections of 100% CO2-saturated saline into the vertebral artery and into the carotid artery. Thirty-nine of the 146 units were excited by the vertebral artery injections in the same time course as ventilatory augmentation. Eighteen of the 39 units did not react to peripheral chemoreceptor stimulation, i.e. they responded exclusively to central chemoreceptor stimulation. These 18 units were distributed in the caudal ('C') chemoceptive area of the ventral surface, in the vicinity of ventral respiratory group (VRG) neurons, and in the dorsal area ventral to the solitary tract. Twenty-one of the 39 units were excited by peripheral chemoreceptor stimulation, i.e. neurons with integrations of central and peripheral chemoreceptor inputs. They were densely packed in the nucleus paragigantocellularis lateralis, although also found in and around the rostral VRG neurons. Fifty-one of the 146 non-phasic units were excited (44) or inhibited (7) immediately after the vertebral artery injections, and their discharges returned to pre-injection levels prior to or during the early period of ventilatory augmentation. They also reacted to skin pinching, i.e. neurons with nociceptive action, and were found scattered variously in the ventral half of the medulla. Fourteen of the 146 units reacted to both chemoreceptor and nociceptor stimulations. The remaining 42 units were non-responsive. In summary, the distributions of the tonically active neurons excited by the central and/or peripheral chemoreceptors were not restricted to the ventral surface of the medulla.

Action Potentials↗
PubMed1989

Stimulation of carotid body chemoreceptors does not influence the discharge of A1 neurons projecting to the forebrain.

Stimulation of carotid body chemoreceptors activates putative vasopressin neurons in the supraoptic nucleus, an effect which has been abolished by lesions in the caudal ventrolateral medulla. Stimulation within the A1 catecholamine cell group in the ventrolateral medulla also activates supraoptic neurons and releases vasopressin. Therefore the A1 catecholamine neurons may be the means by which carotid body chemoreceptors influence the supraoptic nucleus and other parts of the forebrain. To test this possibility the influence of carotid body chemoreceptors on the discharge of rostrally-projecting neurons in the A1 region of the caudal ventrolateral medulla has been assessed in rats anaesthetized with a mixture of urethane and sodium pentobarbitone. Tests were performed on 131 neurons, 23 of which were antidromically invaded following electrical stimulation within the supraoptic nucleus, the medial forebrain bundle or the ventral noradrenergic bundle. The positions of all antidromically invaded neurons were marked with dye and in six animals subsequent fluorescence histochemistry showed that the blue spots were in the proximity of one or more catecholamine-containing cell bodies in the ventrolateral medulla. The recorded neurons were therefore presumed to be part of the A1 group of catecholamine-containing neurons. All neurons located were tested for their responses to specific stimulation of ipsilateral carotid body chemoreceptors and also to general baroreflex activation. Not one of the antidromically invaded neurons was affected by chemoreceptor stimulation and only one was activated by baroreflex activation. Of the non-antidromically invaded neurons, seven were activated and 13 were depressed following chemoreceptor stimulation but in many cases the latency to onset was very long.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed2004

Benzodiazepine-sensitive GABA(A) receptors in the commissural subnucleus of the NTS are involved in the carotid chemoreceptor reflex in rats.

We studied the role of benzodiazepine (BDZ) receptors in the commissural subnucleus of the nucleus tractus solitarius (commNTS) in chemoreceptor reflex in urethane-anesthetized, pancronium-immobilized, artificially ventilated and bilaterally vagotomized rats. A BDZ agonist, diazepam (1-4 micromol/kg), administered intravenously reduced resting phrenic nerve activity (PNA) and blood pressure (BP). Stimulation of carotid chemoreceptors induced an increase in PNA and an increase in BP. Diazepam inhibited this chemoreceptor reflex. The effects of intravenous injection of diazepam (4 micromol/kg) on the chemoreceptor reflex were antagonized by microinjection of the BDZ antagonist flumazenil (100 pmol) into the commNTS. Microinjection of flumazenil (100 pmol) alone had no effect on the basal PNA and BP, and the chemoreceptor reflex. These results suggest that BDZ receptors are present in the carotid chemoreceptor reflex pathway in the commNTS and potentiate GABA(A) transmission.

Animals↗