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PubMed2002

Allosteric enhancement of adaptational demethylation by a carboxyl-terminal sequence on chemoreceptors.

Sensory adaptation in bacterial chemotaxis is mediated by covalent modification of chemoreceptors. Specific glutamyl residues are methylated and demethylated in reactions catalyzed by methyltransferase CheR and methylesterase CheB. In Escherichia coli and Salmonella enterica serovar typhimurium, efficient adaptational modification by either enzyme is dependent on a conserved pentapeptide sequence at the chemoreceptor carboxyl terminus, a position distant from the sites of modification. For CheR-catalyzed methylation, previous work demonstrated that this sequence acts as a high affinity docking site, enhancing methylation by increasing enzyme concentration near methyl-accepting glutamates. We investigated pentapeptide-mediated enhancement of CheB-catalyzed demethylation and found it occurred by a distinctly different mechanism. Assays of binding between CheB and the pentapeptide sequence showed that it was too weak to have a significant effect on local enzyme concentration. Kinetic analyses revealed that interaction of the sequence and the methylesterase enhanced the rate constant of demethylation not the Michaelis constant. This allosteric activation occurred if the sequence was attached to chemoreceptor, but hardly at all if it was present as an isolated peptide. In addition, free peptide inhibited demethylation of the native receptor carrying the pentapeptide sequence at its carboxyl terminus. These observations imply that the allosteric change is transmitted through the protein substrate, not the enzyme.

Allosteric Regulation↗
PubMed2004

Carotid chemoreceptor reflexes following dietary salt loading in rats.

There is a strong association between salt intake and hypertension. Alterations in baroreceptor activity, which precede and contribute to the elevation in blood pressure, have also been shown to affect chemoreceptor reflex response. Dietary salt loading with 8% sodium chloride was carried out in Sprague Dawley rats aged 8 weeks for a period of 5-6 weeks. Blood pressure was thereafter recorded under anaesthesia from the common carotid artery with a Grass Polygraph 7D model, whereas serum Na and K concentrations were measured using a flame photometer. Salt loading resulted in elevated arterial blood pressure as well as hypokalaemia. Stimulation of the carotid chemoreceptor by injection of sodium dithionite resulted in elevated arterial blood pressure, decreased heart rate and hyperventilation in both control and salt-loaded rats. However, the bradycardic response as estimated by the difference in percentage reduction in heart rate was significantly higher in salt rats (36%) than in the control rats (10%). The results indicate that a high-salt diet results in enhanced bradycardic response to carotid chemoreceptor stimulation and that this observation may be related to the attendant hypokalaemia.

Acetic Acid↗
PubMed2000

Olfactory receptor database: a sensory chemoreceptor resource.

The Olfactory Receptor Database (ORDB) is a WWW-accessible database that has been expanded from an olfactory receptor resource to a chemoreceptor resource. It stores data on six classes of G-protein-coupled sensory chemoreceptors: (i) olfactory receptor-like proteins, (ii) vomeronasal receptors, (iii) insect olfactory receptors, (iv) worm chemo-receptors, (v) taste papilla receptors and (vi) fungal pheromone receptors. A complementary database of the ligands of these receptors (OdorDB) has been constructed and is publicly available in a pilot mode. The database schema of ORDB has been changed from traditional relational to EAV/CR (Entity-Attribute-Value with Classes and Relationships), which allows the interoperability of ORDB with other related databases as well as the creation of intra-database associations among objects. This inter-operability facilitates users to follow information from odor molecule binding to its putative receptor, to the properties of the neuron expressing the receptor, to a computational model of activity of olfactory bulb neurons. In addition, tools and resources have been added allowing users to access interactive phylogenetic trees and alignments of sensory chemoreceptors. ORDB is available via the WWW at http://ycmi.med. yale.edu/senselab/ordb/

Base Sequence↗
PubMed1991

Localization of [125I]endothelin binding sites in the region of the carotid bifurcation and brainstem of the cat: possible baro- and chemoreceptor involvement.

We have demonstrated by autoradiography, displaceable binding for [125I]endothelin-1 ([125I]ET-1), [125I]endothelin-2 ([125I]ET-2), and [125I]endothelin-3 ([125I]ET-3) in the cat carotid bifurcation as well as in the nucleus of the tractus solitarius, where baroreceptor and chemoreceptor afferents from the carotid body and sinus terminate. There was also significant binding in the nodose and superior cervical ganglia. Barosensory and chemosensory discharge was recorded from filaments of the carotid sinus nerve in cats anesthetized with pentobarbitone. Intra-carotid injection of ET-1 or ET-3 (4-402 pmoles) caused transient dose-related depression of baroreceptor discharge without any immediate effects on systemic blood pressure (BP) or heart rate; there was a delayed biphasic effect on BP. ET-1 had little effect on chemosensory discharge during the first 15 s post-injection, but there was a delayed (45-90 s) dose-related increase in discharge. The effects of all three ETs were qualitatively similar, and ET enhanced chemoexcitation evoked by either acetylcholine or sodium cyanide. Our results show that (a) ET binding sites are located in the baroreceptor and chemoreceptor afferent pathways and (b) ETs can influence afferent activity of baroreceptors and chemoreceptors. Further studies are needed to determine the significance of these findings, particularly with regard to reflex control of the cardiovascular system.

Animals↗
PubMed2006

The carboxyl-terminal linker is important for chemoreceptor function.

Sensory adaptation in bacterial chemotaxis is mediated by chemoreceptor methylation and demethylation. In Escherichia coli, methyltransferase CheR and methylesterase CheB bind both substrate sites and a carboxyl-terminal pentapeptide sequence carried by certain receptors. Pentapeptide binding enhances enzyme action, an enhancement required for effective adaptation and chemotaxis. Pentapeptides are linked to the conserved body of chemoreceptors through a notably variable sequence of 30-35 residues. We created nested deletions from the distal end of this linker in chemoreceptor Tar. Chemotaxis was eliminated by deletion of 20-40 residues and reduced by shorter deletions. This did not reflect generalized disruption, because all but the most extremely truncated receptors activated kinase, were substrates for adaptational modification and performed transmembrane signalling. In contrast, linker truncations reduced rates of adaptational modification in parallel with chemotaxis. We concluded the linker is important for chemotaxis because of its role in adaptational modification. Effects of linker truncations on CheR binding to receptor-borne pentapeptide implied linker (i) makes pentapeptide available to modification enzymes by separation from the helical receptor body, and (ii) is a flexible arm allowing dual binding of enzyme to pentapeptide and modification site. The data suggest linker and the helix from which it emerges are structurally dynamic.

Amino Acid Sequence↗
PubMed1997

Development of carotid chemoreceptor dynamic and steady-state sensitivity to CO2 in the newborn lamb.

1. The maturation of carotid chemoreceptor steady-state and dynamic responses to CO2 in newborn lambs was measured. In total, sixteen fibres (13 lambs) were studied at 3-4 days, nineteen fibres (13 lambs) at 5-9 days and twenty-one fibres (17 lambs) at 10-24 days after birth. 2. Steady-state CO2 sensitivity was measured over a range of arterial CO2 pressures (Pa,CO2) at four levels of arterial O2 pressure (Pa,O2): hyperoxia (Hyp), 115-150 mmHg; normoxia (Nx), 90-105 mmHg; moderate hypoxia (ModHx), 40-60 mmHg; and severe hypoxia (SvHx), 20-35 mmHg. 3. Steady-state CO2 sensitivity was present at all ages, and a significant effect of age (P < 0.001) and Pa,O2 (P < 0.025) (ANOVA) was observed. Older lambs were unable to sustain an increase in chemoreceptor discharge during SvHx as CO2 was increased. 4. Dynamic CO2 sensitivity was measured by producing alternations in end-tidal CO2 levels (etCO2) (alternation amplitude, 1.23 +/- 0.07% (mean +/- S.E.M.); etCO2, 7.56 +/- 0.15%) over 2-8 s at two Pa,O2 levels only: 80-100 (Nx) and 40-60 mmHg (ModHx). Peak and trough values of the oscillation in chemoreceptor discharge were plotted against maximum and minimum etCO2 for the control and CO2-loaded breaths. Dynamic CO2 sensitivity was calculated as the slope between these points. 5. Dynamic CO2 sensitivity was greater than steady-state sensitivity in Nx (P < 0.05) and ModHx (P < 0.01, Student's paired t test). Unlike steady-state CO2 sensitivity, there was no significant effect of age or Pa,O2 on dynamic sensitivity (P > 0.39 and P > 0.68, respectively, ANOVA). 6. Our results show that the neonatal lamb possesses a carotid body steady-state CO2 sensitivity within a few days of birth, an age when hypoxia sensitivity is low. This CO2 sensitivity increases with age, perhaps due to the increasing interaction between CO2 and O2. Dynamic sensitivity of the carotid body to CO2 is mature at birth and does not increase with age, as predicted if the response of the carotid body to rapid changes in CO2 is independent of the sensitivity to the partial pressure of O2 (PO2).

Aging↗
PubMed1999

Activity of aortic chemoreceptors in the anaesthetized rat.

1. It has been widely accepted that the rat aortic depressor nerve contains only baroreceptors. However, the experiments which have provided these negative data have employed whole aortic nerve recording. In the present study, the technical difficulties associated with recording single fibres in vivo, from the rat aortic nerve (diameter 25-50 microm), have been surmounted using a small tip, glass suction electrode technique. 2. Upon switching from normocapnic hyperoxia to hypercapnic hypoxia, irregularly firing units (n = 13) appeared and these were significantly excited by intravenous injections of sodium cyanide (20 microg) but not by rises in arterial blood pressure induced by methoxamine (an alpha1-adrenoreceptor agonist; 10 microg). Inhalation of 100 % oxygen rapidly and reversibly silenced, or profoundly reduced, ongoing activity. 3. Intravenous injection of phenylbiguanide (PBG; a 5-HT3 receptor agonist; 8 microg) strongly stimulated the chemoreceptors and was followed by a period of chemodepression (3-21 s). In contrast none of the single fibre baroreceptors recorded (n = 15) were excited by PBG but all significantly increased their discharge in response to the increases in arterial blood pressure associated with methoxamine and cyanide. Both the excitatory and inhibitory effects of PBG on the chemoreceptor fibres were abolished by ondansetron (a 5-HT3 receptor antagonist: 1 mg kg-1 i.v.; n = 5 animals) whilst the chemoexcitatory action of cyanide was preserved. 4. It is concluded that there are chemoreceptor afferents contained in the aortic nerve of the Sprague-Dawley rat. The 5-HT3 receptor appears not to be a pre-requisite for aortic body chemoexcitation.

Anesthesia↗
PubMed2001

A pH-sensitive chloride current in the chemoreceptor cell of rat carotid body.

1. Cardiorespiratory response to acidosis is initiated by the carotid body. 2. The direct effect of extracellular pH (pH(o)) on the chloride currents of isolated chemoreceptor cells of the rat carotid body was investigated using the whole-cell patch-clamp technique. 3. On applying intra- and extracellular solutions with a symmetrical high-Cl(-) content and with the monovalent cations replaced with membrane-impermeant ones, an inwardly rectifying Cl(-) current was found. 4. The current activated slowly and did not display any time-dependent inactivation. Current activation was present at membrane potentials negative to 0 mV (pH(o) = 7.0). 5. The current was activated by extracellular acidosis and inhibited by alkalosis in the physiologically relevant pH range of 7.0-7.8. 6. The current was reduced by 0.1 mM Cd2+ to the level of the leak current and by 1 mM anthracene-9-carboxylic acid (9-AC) to about 40 %, while 0.1 mM Ba2+ had no effect. 7. Application of 1 mM 9-AC caused a slow but statistically significant increase in the resting pH(i) (from a mean of 7.29 to 7.37 in 5 min) in clusters of chemoreceptor cells in CO(2)/HCO3(-)-buffered media as measured with carboxy-SNARF-1. 8. When membrane potential changes were estimated in the cell-attached mode, 1 mM 9-AC hyperpolarized three out of five tested cells (by 14 mV in average) incubated in CO(2)/HCO3(-)-buffered media. 9. In summary, chemoreceptor cells express an inwardly rectifying Cl(-) current, which is directly regulated by pH(o). The current may participate in intracellular acidification and membrane depolarization during acidic challenge.

Animals↗
PubMed2001

Reduced to oxidized glutathione ratios and oxygen sensing in calf and rabbit carotid body chemoreceptor cells.

1. The aim of this work was to test the redox hypotheses of O(2) chemoreception in the carotid body (CB). They postulate that hypoxia alters the levels of reactive oxygen species (ROS) and the ratio of reduced to oxidized glutathione (GSH/GSSG), causing modifications to the sulfhydryl groups/disulfide bonds of K+ channel proteins, which leads to the activation of chemoreceptor cells. 2. We found that the GSH/GSSG ratio in normoxic calf CB (30.14 +/- 4.67; n = 12) and hypoxic organs (33.03 +/- 6.88; n = 10), and the absolute levels of total glutathione (0.71 +/- 0.07 nmol (mg tissue)(-1), normoxia vs. 0.76 +/- 0.07 nmol (mg tissue)(-1), hypoxia) were not statistically different. 3. N-Acetylcysteine (2 mM; NAC), a precursor of glutathione and ROS scavenger, increased normoxic glutathione levels to 1.03 +/- 0.06 nmol (mg tissue)(-1) (P < 0.02) and GSH/GSSG ratios to 59.05 +/- 5.05 (P < 0.001). 4. NAC (20 microM-10 mM) did not activate or inhibit chemoreceptor cells as it did not alter the normoxic or the hypoxic release of (3)H-catecholamines ((3)H-CAs) from rabbit and calf CBs whose CA deposits had been labelled by prior incubation with the natural CA precursor (3)H-tyrosine. 5. NAC (2 mM) was equally ineffective in altering the release of (3)H-CAs induced by stimuli (high external K+ and ionomycin) that bypass the initial steps of the hypoxic cascade of activation of chemoreceptor cells, thereby excluding the possibility that the lack of effect of NAC on normoxic and hypoxic release of (3)H-CAs results from a concomitant alteration of Ca(2+) channels or of the exocytotic machinery. 6. The present findings do not support the contention that O(2) chemoreception in the CB is linked to variations in the GSH/GSSG quotient as the redox models propose.

Acetylcysteine↗
PubMed1983

Neonatal breathing control mediated via the central chemoreceptors.

Respiratory changes elicited via the central chemoreceptor system have been studied in anesthetized newborn guinea pigs and newborn rabbits. Periodic breathing was induced by inhibition of the central chemoreceptors by superfusion with alkaline cerebrospinal fluid. The periodic breathing was promptly reversed to steady by increasing the oxygen or carbon dioxide concentration in the inspired air or by intravenous theophylline. Elicitation of periodic breathing simply by exposing the animals to hypoxia succeeded only when very low oxygen concentrations were given. Clearcut respiratory excitation was produced by small amounts of theophylline applied onto the ventral surface of the medulla. Not only theophylline intravenously but also theophylline topically applied on the ventral medullary surface normalized spontaneously developed periodic breathing. Application of meperidine onto the ventral medullary surface gave respiratory inhibition with dosages considerably lower than required when given intravenously. The results emphasize the importance of an adequate respiratory drive from the central chemoreceptors for the maintenance of a regular breathing pattern. The findings support a view that at least part of the respiratory effects seen in the newborn following administration of meperidine or theophylline is due to effect of the drugs on the central chemosensitive system.

Animals↗
PubMed1988

The effect of hypoxia on plasma potassium concentration and the excitation of arterial chemoreceptors in the cat.

Intra-arterial recordings of potassium concentration ([K+]a) and arterial chemoreceptor discharge were made in six anaesthetized cats while tracheal PO2 was stepped every 2 min (end-tidal PO2 ca. 140, 60, 40 and 95 Torr) at constant PCO2 (33 Torr). [K+]a increased hyperbolically from 3.0 mM to 4.5 mM as arterial PO2 was lowered from 95 to 40 Torr. Because the discharge of arterial chemoreceptors is excited by hyperkalaemia as well as hypoxia, the hypoxic discharge of arterial chemoreceptors may have a component mediated by [K+]a. The mechanisms underlying the arterial K+ increase in hypoxia remain unknown.

Action Potentials↗
PubMed2005

Homing in on the specific phenotype(s) of central respiratory chemoreceptors.

To some it may seem that we now know less about respiratory chemoreception than we did 20 years ago. Back then, it was widely accepted that the central respiratory chemoreceptors (CRCs) were located exclusively on or near the surface of the ventrolateral medulla (VLMS). Now, instead, it is generally believed that there are widespread sites of chemoreception, and there is little agreement on when and how each of these sites is involved in respiratory control. However, those in the field know that this actually is progress, primarily because we have gone from simply identifying candidate regions, to identifying specific neuronal subtypes that may be the sensors. In this invited review, we have been asked to discuss some of the current controversies in the field. First, we define the minimal requirements for a cell to be a CRC, and what assumptions can not be made without more data. Then we review the evidence that two neuronal subtypes, serotonergic neurones of the midline raphe and glutamatergic neurones of the retrotrapezoid nucleus, are chemoreceptors. There is evidence supporting a role in respiratory chemoreception for both types of neurone, as well as the other candidates, but there is also information that is missing. Future work will need to focus on which of the candidates are indeed chemoreceptors, what percentage of the overall response each one contributes, and how this percentage varies under different conditions.

Animals↗
PubMed1967

Observations on the rhythmic variation in the cat carotid body chemoreceptor activity which has the same period as respiration.

1. The activity in carotid body chemoreceptor afferent fibres in the cat has been recorded and found to have a rhythm with the same period as respiration.2. This rhythm is not an artifact; it is not due to arterial pressure changes with respiration nor to cyclical changes in pulmonary venous admixture. It is caused by changes in blood gas tensions during each respiratory cycle.3. The amplitude of the rhythm is modified by transient and long-term changes in inspired oxygen or CO(2) so that a rise or fall in O(2) or CO(2) tensions of arterial blood (P(a,O2), P(a,CO2)) from the physiological range reduces it. The ratio of the rhythm amplitude to the mean rate of chemoreceptor discharge increases with P(a,O2) over the range 40-240 mm Hg.4. The rhythm is modified by changes in respiratory frequency and volume.5. The fluctuations of arterial oxygen tension which have the same period as respiration are shown to be conducted up the vertebral artery at least as far as the vertebro-occipital anastomosis.6. It is proposed that the chemoreceptor rhythm reflects the moment to moment changes in blood gas tensions.

Action Potentials↗
PubMed1978

Inhibition of baroreceptor and chemoreceptor reflexes on heart rate by afferents from the lungs.

1. Brief stimuli were delivered to the carotid baroreceptors or chemoreceptors in dogs anaesthetized with chloralose and paralysed with D-turbocurarine. Baroreceptor stimulation was achieved by forceful retrograde injection of 2-5 ml or air-equilibrated saline into the external carotid artery after first clamping the common carotid artery. Chemoreceptor stimulation was achieved by rapid retrograde injections of 0.2-0.5 ml of warmed CO2-equilibrated saline into the external carotid artery. Observations were made during periods of temporary cessation of artificial ventilation. 2. When the volume of the lungs was not changing, prompt decreases in heart rate were evoked by chemoreceptor or baroreceptor stimuli except when these were delivered during the inspiratory phase of breathing (as judged from the records of phrenic nerve activity). 3. No changes in heart rate were evoked when these stimuli were timed to occur during expansion of the lungs in response to a rapid increase in intratracheal pressure (6-10 mmHg in 1-2 sec). Decreases in heart rate were evoked when the stimuli occurred during slower inflations of the lungs. 4. Both stimuli regained their effectiveness on heart rate with time after inflations of the lung when the lungs were held inflated. Both stimuli evoked large decreases in heart rate when delivered during deflations of the lung. 5. The effects of lung inflation on the effectiveness of both cardiodepressor reflexes were abolished by surgical denervation of the lungs.

Animals↗
PubMed1981

Inspiratory inhibition of vagal responses to baroreceptor and chemoreceptor stimuli in the dog.

1. Single and few-fibre cardiac efferent filaments were dissected from the cervical vagus nerve of dogs anaesthetized with chloralose and paralysed with pancuronium. 2. Brief selective baroreceptor or chemoreceptor stimuli, given during the expiratory phase of the central respiratory cycle and while the lungs were motionless, evoked trains of action potentials in cardiac vagal efferent fibres. These vagal responses outlasted the duration of the stimuli by 1-3 s. 3. Brief selective baroreceptor or chemoreceptor stimuli given during the inspiratory phase of the central respiratory cycle (monitored as phrenic discharge) but while the lungs were motionless, failed to evoke reflex increases in discharge. Background vagal discharge was also inhibited during central inspiratory activity. 4. Brief baroreceptor or chemoreceptor stimuli given during lung inflation but in the expiratory phase of the central respiratory cycle (phrenic silence), also failed to evoke any reflex increase in discharge, but left resting vagal tone relatively unaffected. Only when vagal tone was high was it markedly inhibited by lung inflation, in the absence of central inspiratory activity. 5. A point of contrast between the inhibitory effects of lung inflation and of central inspiratory activity is that both tonic and reflexly evoked vagal discharge are inhibited during central inspiratory activity, but lung inflation more markedly inhibits reflexly evoked vagal discharge than tonic vagal discharge. 6. A model is suggested to explain the different mechanisms of inhibition by lung inflation and by central inspiratory activity.

Animals↗
PubMed1981

Arterial chemoreceptor-like activity in the abdominal vagus of the rat.

1. Centripetal activity in fibres in the ventral abdominal vagus nerve of the rat has been studied by recording from fine strands of the divided nerve within the abdomen. 2. In the starved animal, few spontaneously active fibres were located. A proportion of these, however, showed changes in activity in response to changes in F1 oxygen which were typical of arterial chemoreceptor afferent nerves. The resting discharge in these preparations was 0.8-8.0 impulses/sec. In response to extreme hypoxic hypoxia, histotoxic hypoxia or acetylcholine, this discharge increased markedly, with a maximum mean activity of up to 25 impulses/sec. 3. Both the mean/S.D. ratio and statistical comparison with a 'noise' equation were used to assess the apparent random nature of the spike intervals. The former indicated that the spike intervals were random but the latter test was inconclusive. 4. We suggest that this chemoreceptor-like activity originates from the abdominal vagal paraganglia and that these structures may be part of a more generally distributed chemoreceptor system.

Abdomen↗
PubMed1983

Responses of abdominal vascular resistance and capacitance to stimulation of carotid chemoreceptors in anaesthetized dogs.

1. In anaesthetized dogs the regions of the carotid bifurcations were isolated vascularly and perfused at constant non-pulsatile pressures. The abdominal circulation was isolated vascularly, perfused at constant flow and drained through the inferior vena cava at constant pressure. Vascular resistance and capacitance responses were determined from the changes in perfusion pressure and changes in venous outflow. 2. Stimulation of carotid chemoreceptors with venous blood resulted in an increase in arterial perfusion pressure of 38% (S.E. +/- 4.6) and a decrease in vascular capacitance of 24.4 +/- 2.5 ml. (1.05 +/- 0.24 ml. kg-1). 3. When carotid perfusion pressure was higher than 17 kPa, stimulation of chemoreceptors resulted in significantly (P less than 0.05) smaller resistance responses but significantly (P less than 0.05) greater capacitance responses than those obtained at lower carotid pressures. 4. These results show that abdominal resistance and capacitance vessels constrict in response to stimulation of carotid chemoreceptors. We suggest that the larger responses of capacitance and the smaller responses of resistance obtained at higher carotid sinus pressures may be due to different sensitivities of resistance and capacitance vessels to efferent sympathetic nerve activity.

Abdomen↗
PubMed1987

The effects of stimulating carotid chemoreceptors on renal haemodynamics and function in dogs.

1. Dogs were anaesthetized with chloralose and artificially ventilated. The carotid chemoreceptors were stimulated by changing the perfusion of vascularly isolated carotid sinus regions from arterial to venous blood. The mean carotid sinus pressure and the mean arterial blood pressure were held constant at 124 +/- 3 and 122 +/- 3 mmHg, respectively. Both vagosympathetic trunks were sectioned in the neck and propranolol (17 micrograms kg-1 min-1 I.V.) and gallamine triethiodide (0.2-2.0 mg kg-1 30 min-1 I.V.) were infused. Renal blood flow was measured by an electromagnetic flow probe, glomerular filtration rate by creatinine clearance, sodium excretion by flame photometry and solute excretion by osmometry. 2. In sixteen tests in thirteen dogs perfusion of the carotid sinus regions with venous blood resulted in significant decreases in renal blood flow from 271 +/- 24 to 198 +/- 21 ml min-1 100 g-1 renal mass; glomerular filtration rate from 41.0 +/- 4.8 to 22.1 +/- 3.1 ml min-1 100 g-1; filtration fraction from 0.25 +/- 0.02 to 0.19 +/- 0.02; urine flow from 0.48 +/- 1.0 to 0.21 +/- 0.03 ml min-1 100 g-1; sodium excretion from 18.1 +/- 4.1 to 12.9 +/- 4.2 mumol min-1 100 g-1; and osmolar excretion 327 +/- 42 to 171 +/- 26 mu osmol min-1 100 g-1. The right atrial pressure did not change significantly from 4.6 +/- 1.2 cmH2O. 3. In seven dogs, tying renal sympathetic nerves abolished all the responses except that of sodium excretion which was now reversed; sodium excretion increased from 68 +/- 19 to 116 +/- 38 mumol min-1 100 g-1 without significant change in right atrial pressure from 7.4 +/- 1.9 cmH2O. Crushing the carotid bodies, however, abolished all the responses. 4. The results show that carotid chemoreceptor stimulation can cause significant reflex effects on renal haemodynamics and function which are mediated via renal sympathetic nerves. They also show that the chemoreceptor stimulation can cause natriuresis in the absence of haemodynamic changes, in the denervated kidney, presumably via a humoral factor.

Animals↗