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At least 19 recordsLinked to original sources
PubMed1974

Interaction of baroreceptor and chemoreceptor reflexes. Modulation of the chemoreceptor reflex by changes in baroreceptor activity.

The purpose of this study was to determine whether the level of arterial pressure and degree of baroreceptor activation affect responses to stimulation of chemoreceptors. Chemoreceptors were stimulated by injecting nicotine into the common carotid artery of anesthetized and paralyzed dogs. Responses were observed in the innervated gracilis muscle, perfused at constant flow while perfusion pressure was measured. Arterial pressure was lowered by bleeding the animals and raised by transient occlusion of the descending aorta. Vasoconstrictor responses to stimulation of chemoreceptors were enhanced by hypotension and inhibited by elevation of arterial pressure. Potentiation of the chemoreceptor reflex by hemorrhagic hypotension was not the result of altered vascular resistance in the gracilis muscle, sensitization of chemoreceptors by catecholamines or acidosis, or changes in cerebral perfusion pressure. Additional studies were done in which we excluded the possibility that the changes resulted from direct effects of changes in arterial pressure on chemoreceptors. Both carotid bifurcations were isolated and perfused. On one side, pressure was raised to stimulate the carotid sinus baroreceptors. On the other side, the carotid body chemoreceptors were stimulated by nicotine or by hypoxic and hypercapnic blood. Activation of baroreceptors on one side attenuated the vasoconstrictor response to chemoreceptor stimulation on the other side. This excludes a direct effect of changes in arterial pressure on the chemoreceptors and suggests a central interaction of these reflexes. We conclude that vasoconstrictor responses to stimulation of chemoreceptors are potentiated by hypotension and inhibited by transient hypertension. These effects appear to result at least in part from a central interaction of chemoreceptor and baroreceptor reflexes.

Animals↗
PubMed1981

Interaction between the responses to stimulation of peripheral chemoreceptors and baroreceptors: the importance of chemoreceptor activation of the defence areas.

It has been shown recently that in the cat anesthetized with althesin, stimulation of carotid chemoreceptors evokes the autonomic components of the alerting stage of the defence reaction including cholinergic vasodilatation in skeletal muscle. The discrepancy between this result and those of previous experiments on animals anethetized with chloralose or barbiturates may be reconciled when it is realized that these more conventional anesthetics prevent normal transmission through the defence areas. The obvious conclusion, that activation of the defence area is an integral part of the response to peripheral chemoreceptor stimulation indicates that the question of interaction between baro- and chemoreceptor responses should be reconsidered, particularly as it is known that the baroreceptor reflex is suppressed when the defence areas are activated by central stimulation. The present paper describes experiments performed on Althesin-anesthetized cats in which carotid baroreceptors were stimulated by inflating a blind sac and carotid chemoreceptors were stimulated by injections of inorganic phosphate solution or saline equilibrated with CO2. The results showed that the baroreceptor reflex may be fully suppressed when the autonomic components of the alerting response were evoked by chemoreceptor stimulation. In some cases however, when the activation of the defence areas was mild, at least as judged by the magnitude of the cholinergic vasodilatation evoked by the chemoreceptor stimulus alone, there appeared to be algebraic summation of the baro- and chemoreceptor response. It is concluded that the extent to which a given chemoreceptor stimulus suppresses the baroreceptor reflex is dependent on its potency as a stimulus to the defence areas. It is suggested that the chemoreceptor input may be more important than hitherto suspected in setting the level of arterial blood pressure.

Animals↗
PubMed1985

Kidney function during arterial chemoreceptor stimulation. I. Influence of unilateral renal nerve section, bilateral cervical vagotomy, constant artificial ventilation, and carotid body chemoreceptor inactivation.

The reactions of renal hemodynamics and excretory function elicited by perfusion of the vascularly isolated carotid bodies with venous blood were studied in four groups of chloralosed cats in which the Nn. vagi, the breathing reactions, and the carotid body chemoreceptors were excluded successively. The kidney function was determined using clearance-techniques in both the innervated right and denervated left kidneys. In the animals with intact carotid chemoreceptors perfusion of the carotid bifurcations with venous blood caused a weak (4-6 mm Hg on the average) and transient increase of the mean systemic arterial blood pressure as well as a vasoconstriction and a fall of the blood flow and glomerular filtration rate in the innervated kidneys. In the spontaneously breathing animals carotid body chemoreceptor stimulation effected a rise of fractional sodium excretion only in the denervated kidneys whereas the relaxed and constantly ventilated cats showed a natriuretic response both at the innervated and denervated side. The reactions of renal excretory function did not correlate with those of renal hemodynamics. Vagotomy, relaxation, and constant artificial ventilation failed to abolish the responses elicited by stimulation of the chemoreceptors. Inactivation of the carotid body chemoreceptors by injecting acetic acid into the vascularly isolated carotid sinuses prevented both the hemodynamic and tubular reactions due to hypoxic-hypercapnic perfusion of the carotid bodies. The findings suggest that the arterial chemoreceptors control kidney function by specific reflex mechanisms. The influence of the carotid body chemoreceptors on kidney vasculature is mediated by the efferent renal nerves, whereas the control of renal tubular sodium reabsorption requires hormone action.

Animals↗
PubMed1985

Kidney function during arterial chemoreceptor stimulation. III. Long-lasting inhibition of renal tubular sodium reabsorption due to pharmacologic stimulation of the peripheral arterial chemoreceptors with almitrine bismesylate.

The reactions of the mean systemic arterial blood pressure, arterial acid-base balance kidney function (clearance-technique), and plasma aldosterone concentration (radio-immunoassay) elicited by stimulation of the peripheral arterial chemoreceptors with almitrine bismesylate were determined in chloralosed, non-vagotomized, spontaneously breathing cats in moderate mannitol-saline diuresis. The left renal nerves were cut; urine was collected separately from both the innervated and denervated kidneys. Intravenous injection of 0.2 mg/kg of the drug caused the expected long-lasting increase of the pO2 and pH and a decrease of pCO2 in the arterial blood, whereas the mean systemic arterial blood pressure slightly rose by an average of 2-4 mm Hg in the first hour of chemoreceptor stimulation but afterwards considerably decreased below the pre-injection values. The renal responses were characterized by a moderate vasoconstriction particularly in the innervated kidneys and a pronounced increase of sodium and urine excretion especially in the denervated kidneys. The inhibition of renal tubular sodium reabsorption underlying these natriuretic and diuretic reactions was fully demonstrable even at the end of the experiments, i. e. 4 h after the administration of the agent. Plasma aldosterone increased with the time of the experiments but did not show any clear relationships to the activity of the arterial chemoreceptors. The results show that the intravenous injection of almitrine bismesylate is connected with a renal response pattern which is typical for an excitation of the peripheral arterial chemoreceptors, i. e. moderate vasoconstriction (efferently mediated by the renal nerves) and an inhibition of renal tubular sodium reabsorption (efferently mediated by hormonal mechanisms). Furthermore, the data suggest that, on the one hand, under certain conditions these reactions of the kidney function could play the role of undesirable side effects but, on the other hand, the inhibition of renal tubular sodium reabsorption caused by almitrine bismesylate might possibly be used to treat diseases that are connected with a reduced ability of the kidneys to sufficiently excrete sodium.

Aldosterone↗
PubMed1987

Carotid chemoreceptor discharge responses to hypoxia and hypercapnia in normotensive and spontaneously hypertensive rats.

The carotid chemoreceptor discharge responses to hypoxia and hypercapnia were quantitatively compared between normotensive (NTR) and spontaneously hypertensive rats (SHR). For this purpose we recorded afferent mass discharges from the carotid sinus nerve (CSN) at various levels of end-tidal O2 and CO2 concentrations (FetO2, FetCO2 (%)) in the urethane-anesthetized, vagotomized and artificially ventilated rats. The CSN chemoreceptor discharge was evaluated by subtracting the small activity remaining in acute hyperoxia (chemoreceptor inactivation), which was estimated as baroreceptor in origin, from the large total CSN activity. The CSN chemoreceptor discharges at various levels of FetO2 or FetCO2 were expressed as the percent of control activity measured in normoxic and normocapnic conditions (FetO2, 15-16%; FetCO2, 4.5-5.1%). There was an exponential increase in the CSN chemoreceptor discharge as FetO2 was decreased from hyperoxic to various hypoxic levels (maximally 6%) at a maintained FetCO2 (normocapnia). The relationship between the CSN chemoreceptor discharge and the hypoxic stimulus was quantitatively assessed by the regression analysis using an exponential function. Exponential increases in the CSN chemoreceptor discharge by hypoxia and the parameters in the exponential function reflecting the sensitivity to hypoxia were significantly higher in the SHR than in the NTR, which indicated a high carotid chemoreceptor discharge response to hypoxia in the SHR. The CSN chemoreceptor discharge was increased linearly by increasing the FetCO2 from the normocapnic level up to about 10% at a maintained FetO2 (normoxia). Increases in discharge produced by severe hypercapnia were, however, much smaller than that caused by hypoxia. The slope of the CO2 stimulus-CSN chemoreceptor discharge response line was almost the same in NTR and SHR. The results demonstrated that the responsiveness of rat carotid chemoreceptor to hypoxia is augmented in the SHR. The role of carotid chemoreceptor afferents in ventilatory reflex responses to hypoxia and their alterations in the SHR are discussed.

Animals↗
PubMed1975

The action of 5-hydroxytryptamine on chemoreceptor discharges of the cat's carotid body.

1 Chemoreceptor discharges were recorded in vivo from fine filaments of the carotid sinus nerve containing a single or several active units; their frequency was used as an index of receptor activity. The effects of 5-hydroxytryptamine (5-HT) on chemoreceptors were studied in 26 adult cats. At times, sinus baroreceptor discharges were recorded from the carotid nerve and the effect of 5-HT on the discharges was examined. 2 Intra-carotid injections of 5-HT (2-20 mug) induced a sharp and brief increase in chemoreceptor discharges, followed by depression or block which lasted for several seconds. Repeated injections at short intervals, and a small dose after a large dose of 5-HT resulted in depressed or blocked response to 5-HT. 3 5-HT in high doses (10-20 mug, i.a.) slightly depressed the chemoreceptor discharges induced by either acetylcholine (ACh) or NaCN, when these substances were applied within 20 s after 5-HT. 5-HT (5-20 mug, i.a.) applied during asphyxia induced a further increase in chemoreceptor discharges, soon followed by block of the discharges lasting for several seconds. 4 Atropine or hexamethonium in high doses did not change the chemoreceptor response to 5-HT, while that to ACh was markedly depressed. 5 (+)-Lysergic diethylamide (LSD), methysergide or gramine did not alter the response to 5-HT, while LSD in low doses produced a marked increase in chemoreceptor discharges. 6 Acute and chronic treatment with reserpine (5-10 mg/kg, i.v.) of the animals did not change the sensitivity and the reactivity of the chemoreceptor to ACh and NaCN, while the chemoreceptor response to 5-HT was augmented, indicating an increase in the sensitivity of chemoreceptors to 5-HT. 7 5-HT in small doses (2-10 mug, i.a.) induced a marked increase in sinus baroreceptor discharges; subsequently discharges were depressed or blocked for several seconds. 8 The results are discussed in relation to possible mechanism of action of 5-HT on the chemoreceptors. It is concluded that the exogenous 5-HT probably acts directly on the chemosensory nerve endings and depolarizes them, but 5-HT contained in the carotid body does not play a significant role in the generation of chemoreceptor discharges.

Acetylcholine↗
PubMed1985

Kidney function during arterial chemoreceptor stimulation. II. Suppression of plasma aldosterone concentration due to hypoxic-hypercapnic perfusion of the carotid bodies in anaesthetized cats.

The reactions of the mean systemic arterial blood pressure, kidney function (clearance technique) and plasma aldosterone concentration (radio-immuno-assay) elicited by perfusion of the vascularly isolated carotid bodies with venous blood were studied in two series of chloralosed, vagotomized, relaxed, and constantly ventilated cats undergoing saline diuresis. In one group of animals the carotid body chemoreceptors were left intact; in the other one, they were abolished by injecting acetic acid into the glomera carotici. In the cats with intact chemoreceptors perfusion of the carotid bodies with venous blood immediately caused a small and transient increase of the blood pressure, whereas renal plasma flow tended to fall despite continuous chemoreceptor stimulation. Renal fractional sodium excretion already increased in the first 25 min of chemoreceptor stimulation, whereas plasma aldosterone concentration showed a significant decrease only after 45 min of venous perfusion of the glomera carotici. Plasma electrolytes changed only little at that time. No clear relationships between the responses of plasma aldosterone and those of the other parameters measured could be obtained. On subsequent perfusion of the carotid bodies with arterial blood plasma aldosterone returned to the values determined before chemoreceptor stimulation. Inactivation of the carotid body chemoreceptors per se already enhanced plasma aldosterone concentration. Perfusion of the glomera carotici with venous blood in the cats with abolished chemoreceptors did not suppress plasma aldosterone content. The data show that plasma aldosterone changes are not involved in the development of the initial phase (first hour) of the inhibition of renal tubular sodium reabsorption provoked by arterial chemoreceptor stimulation, but during long-lasting chemoreceptor stimulation they might contribute to the maintenance of this type of natriuresis. Furthermore the experiments suggest that the decrease of plasma aldosterone repeatedly observed during exposure of mammals to acute hypoxic hypoxia is possibly the reflex result of the stimulation of the arterial chemoreceptors.

Aldosterone↗
PubMed1967

Carotid body chemoreceptor activity in the new-born lamb.

1. Tidal volume, carotid artery oxygen tension (P(a,O2)) and blood pressure and chemoreceptor activity in the sinus nerve have been continuously measured and recorded in nine lambs anaesthetized with pentobarbitone sodium, and varying in age from some minutes after birth to 5 days after birth.2. Inhalation of 100% oxygen caused, after a delay of 3-4 sec, a rise in P(a,O2), a fall in minute ventilation (V) and chemoreceptor activity. The respiratory response was abolished after section of both sinus nerves.3. Inhalation of 10% oxygen in nitrogen caused a fall in carotid P(a,O2), a rise in respiration and in chemoreceptor activity. The respiratory response was abolished after both sinus nerves had been cut.4. Minute ventilation, carotid P(a,O2) and chemoreceptor activity increased on breathing 5% CO(2) in air. Section of both sinus nerves did not affect the maximum increase in ventilation but the lag of the respiratory response approximately doubled while respiration increased more slowly.5. From these results, it was calculated that the chemoreceptors had a latency of 0.25-0.5 sec and the time constant of the rate of change of chemoreceptor activity was 10-15 sec.6. The chemoreceptors responded to changes in P(a,O2) of +/-5-10 mm Hg.7. Comparison of these results with those reported in adult animals suggest that the peripheral chemoreceptors are fully mature at birth, that their response does not differ with the age of the lamb and that the carotid body chemoreceptors are concerned both in the mediation of the hypoxic drive to ventilation and in the respiratory response to inhaled CO(2).

Action Potentials↗
PubMed1971

The effects of electrical stimulation of the distal end of the cut sinus and aortic nerves on peripheral arterial chemoreceptor activity in the cat.

1. In anaesthetized cats, stimulation of efferent components of the carotid sinus or aortic nerves depressed chemoreceptor discharge from the relevant chemoreceptor afferents. The local application of 2% procaine hydrochloride to the sinus nerve trunk, peripheral to the site of the stimulating electrodes and proximal to that of the afferent nerve twig, abolished the depression of afferent chemoreceptor discharge caused by electrical stimulation; on washing the procaine away electrical stimulation once more induced depression of chemoreceptor discharge.2. The depressant effect of efferent stimulation on carotid chemoreceptor activity was still seen during complete carotid glomeral ischaemia. Atropine given by close intra-arterial injection to the carotid body did not affect the depressant influence of efferent sinus nerve stimulation on carotid body chemoreceptor discharge.3. Stimulation of the sinus nerve efferents usually increased carotid body blood flow. Close arterial injection of atropine abolished this effect.4. The responses of glomeral blood flow and carotid chemoreceptor activity to efferent stimulation of the cut sinus nerve were not temporally related. It seems improbable that the depressant effect of such stimulation on chemoreceptor discharge was due to alterations of glomeral blood flow.5. Stimulation of the peripheral end of the cervical vagus in atropinized cats reduced chemoreceptor activity recorded in the ipsilateral aortic nerve.

Animals↗
PubMed1992

Respiratory muscle recruitment during selective central and peripheral chemoreceptor stimulation in awake dogs.

1. In four awake dogs we measured EMG activity of three inspiratory and four expiratory muscles during sustained central chemoreceptor stimulation (CO2 inhalation), and peripheral chemoreceptor stimulation (intravenous infusion of almitrine bismesylate (almitrine)). By using this selective pharmacological stimulation of the peripheral chemoreceptors and reversibly cold-blocking pulmonary stretch receptors, we were able to determine the effects of each type of stimulation on respiratory muscle recruitment in the absence of such complicating influences as pulmonary stretch receptor feedback, cerebral hypoxia or hypocapnia, and differences in breathing pattern. 2. During 10 min of steady-state hyperpnoea (minute ventilation VI, approximately twice eupnoea) caused by either hypercapnia or isocapnic stimulation of the carotid bodies with almitrine, all three inspiratory and all four expiratory muscles demonstrated significant and sustained elevations in EMG activity. 3. With both types of chemoreceptor stimulation, as tidal volume, VT, increased, so did the mean electrical activities of the crural diaphragm (r = 0.88), costal diaphragm (r = 0.93), parasternals (r = 0.82), triangularis sterni (r = 0.74), transversus abdominis (r = 0.77), external obliques (r = 0.68) and internal intercostals (r = 0.75). 4. In each dog, the response of ventilation and of the diaphragmatic EMG to a given level of central or peripheral chemoreceptor stimulation is highly reproducible from one test day to the next. On the other hand, accessory inspiratory and expiratory abdominal and rib cage muscles in two of the four dogs showed highly significant changes from day to day in the amount of their EMG activity at any given VT. 5. During steady-state ventilatory stimulation, 2 min intervals were chosen during which the two types of chemoreceptor stimulation had caused hyperpnoeas with similar values for VT, total time per breath (TTOT) and inspiratory time divided by the total time (TI/TTOT). Comparison of EMG activities during these matched hyperpnoeas revealed that there were no differences in the activities of any of the muscles between the two forms of stimulation. We conclude that peripheral chemoreceptor stimulation causes significant and sustained recruitment of expiratory muscles even in the absence of pulmonary feedback and that both expiratory and inspiratory muscles are recruited to the same extent during peripheral chemoreceptor stimulation as they are during an identical hyperpnoea caused by central chemoreceptor stimulation.

Almitrine↗
PubMed1987

Chemoreceptors of crustaceans: similarities to receptors for neuroactive substances in internal tissues.

A description is given of crustacean chemosensory systems and the neurophysiological procedures used to study them. Their response properties and tuning characteristics are discussed. A review is then provided of specific crustacean chemoreceptors that are stimulated selectively by either purine nucleotides, taurine, glutamate, or glycine, all of which have neuroactive properties in internal tissues. Two distinctly different types of purinergic chemoreceptors occur on the antennules of the spiny lobster. P1-like chemoreceptors have a potency sequence of AMP greater than ADP greater than ATP greater than adenosine and show a strict structural requirement for the ribose phosphate moiety. P2-like chemoreceptors have a potency sequence of ATP greater than ADP greater than AMP or adenosine and show a broad sensitivity to nucleotide triphosphates with modifications in both the purine and ribose phosphate moieties. Sensilla containing the dendrites of chemosensory neurons also possess an ectonucleotidase(s) that inactivates excitatory nucleotides to yield adenosine which is subsequently internalized by a sensillar uptake system. Narrowly tuned taurinergic chemoreceptors are present on both the antennules and legs of lobsters. Although taurine itself is the most effective stimulant, the taurine analogs hypotaurine and beta-alanine are also very excitatory. Structure-activity studies indicate these chemoreceptors have marked similarities to taurine-sensitive systems in internal tissues of vertebrates. By contrast, comparative studies of glutamatergic chemoreceptors on the legs of lobsters indicate response spectra different from those of the glutamate receptors in lobster neuromuscular junctions and the three classes of excitatory amino acid receptors identified internally in vertebrates. Crustacean chemoreceptors for glycine, ecdysteroids, and pyridine are also described. The hypothesis that receptors for internal neuroactive agents may have originally evolved as external chemoreceptors of primitive aquatic organisms is discussed.

Animals↗
PubMed1990

Influence of sorbitol and mannitol on the reactions of kidney excretory function evoked by arterial chemoreceptor stimulation with almitrine in anaesthetized and artificially ventilated cats.

The reactions of renal hemodynamics, as well as of excretory and concentrating function (clearance-technique) in response to arterial chemoreceptor stimulation by almitrine bismesylate were studied in 3 groups of chloralosed, relaxed, and constantly ventilated cats. In 2 groups of chemoreceptor-intact animals an osmotic diuresis was induced by intravenous infusion of an isoionic solution containing equivalent amounts of either sorbitol or mannitol. Under similar conditions the 3rd series of experiments was carried out in cats under mannitol diuresis but with deafferented arterial chemoreceptors. The changes of mean arterial and central venous pressures as well as of the parameters of the arterial acid-base balance were similar in all groups of cats studied. The chemoreceptor-intact animals undergoing sorbitol diuresis did not show any natriuresis in response to the drug but reacted with a remarkable increase in their U/Posm and TCH2O/Cosm ratios. In contrast, the chemoreceptor-intact animals infused with mannitol in saline reacted to almitrine with a transient natriuresis but with only a weak increase in their U/Posm and TCH2O/Cosm ratios. The data suggest that arterial chemoreceptor stimulation inhibits proximal tubular sodium reabsorption. In the sorbitol-experiments during chemoreceptor stimulation the enhanced delivery of sodium by the proximal fluid was reabsorbed in the thick ascending limb of Henle's loop thus increasing medullary osmolality and renal concentrating ability. Mannitol apparently limited this additional sodium reabsorption in the thick ascending limb of Henle's loop; therefore in the mannitol-experiments during chemoreceptor stimulation a natriuresis but only relatively weak changes of renal concentrating function occurred. The data also suggest that a pharmacological chemoreceptor stimulation might support the recovery of renal excretory function post-anaesthetically, although the optimal solution infused to induce an osmotic diuresis remains to be determined.

Almitrine↗
PubMed1988

Carotid body chemoreceptor and ventilatory responses to sustained hypoxia and hypercapnia in the cat.

To understand the role of carotid chemoreceptor activity in the ventilatory responses to sustained hypoxia (30 min) the following measurements were made in cats anesthetized with alpha-chloralose: (1) carotid chemoreceptor and ventilatory responses to isocapnic hypoxia and to hypercapnia during hyperoxia; (2) carotid chemoreceptor responses to isocapnic hypoxia after dopamine receptor blockade; and (3) ventilatory responses to hypoxia after bilateral section of carotid sinus nerves (CSN). Transition to hypoxia (PaO2 approximately equal to 52 Torr) from hyperoxia gradually increased carotid chemoreceptor activity by ten fold and ventilation by two fold without any detectable overshoot. Termination of isocapnic hypoxia with hyperoxia (PaO2 greater than 300 Torr) at 30 min promptly restored the carotid chemoreceptor activity to prehypoxic level. Ventilation also decreased promptly, but remained above the control value. Induction of hypercapnia (from 31.8 Torr to 43.9 Torr) during hyperoxia was followed by a prompt increase in the chemoreceptor activity by four fold which subsequently diminished, and by a gradual four fold increase in ventilation. Termination of hypercapnia after 30 min was followed by a prompt return of chemoreceptor activity and by a slow return of ventilation to near control levels. Dopamine receptor blockade increased carotid chemoreceptor responsiveness to acute hypoxia but did not alter the response pattern during sustained hypoxia. After bilateral CSN section, ventilation decreased during maintained hypoxia. Thus, a stimulatory peripheral and inhibitory central effects of hypoxia could produce a biphasic ventilatory response to short-term hypoxia in the anesthetized cat with intact CSN but did not manifest it. The results suggest that the chemosensory input not only promptly stimulates ventilation but also prevents the subsequent depressant effect of hypoxia on the brain-stem respiratory mechanisms and hence presumably a biphasic ventilatory response in the anesthetized cat.

Animals↗
PubMed1991

Effects of central and peripheral chemoreceptor stimulation on ventilation in the marine toad, Bufo marinus.

The contributions of central and peripheral chemoreceptors to respiratory control in lightly anesthetized Bufo marinus, were assessed by measuring the ventilatory responses to unidirectional ventilation (UDV) of the lungs at several concentrations of CO2 or O2, during intracranial perfusion (ICP) with hypercapnic acidic (5% CO2, pH 7.2) or hypocapnic alkaline (0% CO2, pH 8.3) mock CSF solutions. Peripheral chemoreceptor stimulation alone (hypoxia or hypercapnia during ICP with hypocapnic alkaline CSF) significantly increased breathing frequency and amplitude. ICP with hypercapnic acidic CSF further stimulated ventilation, primarily by significantly increasing the number of breaths/bout of breathing and decreasing the non-ventilatory time at all levels of peripheral ventilatory drive. When peripheral and central chemoreceptor stimulation was low toads were apneic. Stimulation of either central or peripheral chemoreceptors was sufficient to reinitiate breathing. Responses to ICP were greatest when perfusion was directed to the ventral medullary surface (VMS). These results suggest that the initiation of breathing and overall levels of breathing are functions of the combined afferent input from peripheral chemoreceptors and central CO2/pH sensitive chemoreceptors, located near the VMS. Stimulation of central chemoreceptors, however, produced longer duration bouts of rhythmic breathing than did peripheral chemoreceptor stimulation.

Animals↗
PubMed1978

Effects of droperidol on activity of carotid body chemoreceptors in cat.

1 The effect of droperidol on the spontaneous activity of carotid body chemoreceptors and on their response to various stimuli was studied in 21 anaesthetized, paralyzed and artificially ventilated cats. Carotid body blood flow was controlled with a perfusion pump, and drugs were injected into the perfusion circuit. 2 In low doses, droperidol transiently increased the rate of spontaneous chemoreceptor activity, but in higher doses it depressed chemoreceptor activity after an initial stimulation. 3 Droperidol reduced or abolished the normal increase in chemoreceptor activity produced by stagnant asphyxia. This effect did not depend solely on the ability of droperidol to suppress spontaneously occurring impulses. Chemoreceptor responses to sodium cyanide, and to dopamine were also inhibited. 4 Dopamine antagonists other than droperidol were also studied for their effect on chemocreceptor activity. Chlorpromazine depressed spontaneous chemoreceptor activity and also reduced the chemoreceptor responses to sodium cyanide and dopamine, as did pimozide. The effects of these dopamine antagonists were much briefer and less marked than those of droperiodol. 5 Although the influence that we have shown droperidol to have on peripheral chemoreceptor activity has an uncertain basis, it may have important implications in human and veterinary medicine.

Animals↗
PubMed1976

Studies on the central integration of excitatory chemoreceptor influences and inhibitory baroreceptor and cardiac receptor influences.

Experiments were performed on cats to explore the integrated cardiovascular responses when excitatory (chemoreceptor) and inhibitory (baroreceptor or cardiac receptor) influences are simultaneously presented to the medullary cardiovascular areas. At a given sinus pressure in the low or medium pressure range, the systemic blood pressure and the vascular resistance were higher when the chemoreceptors were stimulated, while a high, pulsating sinus pressure, i.e.a strong baroreceptor stimulation, could suppress completely even an intense chemoreceptor activation. Thus, the set point and the gain of the baroreflex were increased by a concomitant chemoreceptor activation. These effects are compatible with a simple, mutual 'summation' of excitatory and inhibitory influences on a common population of central vasomotor neurons. The reflex vasodilator effects elicited via vagal cardiac afferents were found to be more effectively suppressed by a concomitant chemoreceptor stimulation than were the baroreceptor effects, provided a primary chemoreceptor response (bradycardia) was at hand, while the heart rate responses were essentially uninfluenced by the prevailing chemoreceptor activity. This chemoreceptor suppression of the reflex vasodilatation from cardiac receptors, which may be of great importance in hypoxic situations, e.g. during a dive, suggests a more complex, neuronal interaction between the two reflex mechanisms in the CNS.

Afferent Pathways↗