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PubMed1983

Aortic and carotid chemoreceptor responses to metabolic acidosis in the cat.

The effect of metabolic acidosis on the activity of aortic chemoreceptor afferents and their responses to hypoxia and hypercapnia were investigated in nine cats anesthetized with alpha-chloralose, paralyzed, and artificially ventilated. This effect was compared with that on simultaneously recorded activity of carotid chemoreceptor afferents in three separate cats. The activity of a single or paucifiber preparation of chemoreceptor afferents was recorded at five steady-state levels of arterial O2 tension (PaO2) at a constant arterial CO2 tension (PaCO2) and at three levels of PaCO2 during hyperoxia (PaO2 greater than 400 Torr) before and after slow injection of 1 M lactic acid in the average dose of 2.6 +/- 0.6 mmol X kg-1. On the average, arterial pH decreased from 7.445 +/- 0.046 to 7.222 +/- 0.041 at PaO2 of 98 +/- 5 Torr and PaCO2 of 34 +/- 1 Torr. This decrease in pHa during normoxia increased the aortic chemoreceptor activity from 0.8 +/- 0.2 to 1.4 +/- 0.3 imp X s-1. Metabolic acidosis increased the excitatory effect of hypoxia and hypercapnia. The stimulatory effect of CO2 for the same increase in arterial [H+] was greater than that of metabolic acidosis, indicating a dominant effect of molecular CO2 on aortic chemoreceptors. Simultaneous measurements of carotid and aortic chemoreceptor activities showed that their responses to metabolic acidosis were qualitatively similar. Quantitatively, the response of aortic chemoreceptor afferents was less than that of carotid chemoreceptors.

Acidosis↗
PubMed1975

Effect of baroreceptor activity on ventilatory response to chemoreceptor stimulation.

This study tested the hypothesis that ventilatory responses to chemoreceptor stimulation are affected by the level of arterial pressure and degree of baroreceptor activation. Carotid chemoreceptors were stimulated by injection of nicotine into the common carotid artery of anesthetized dogs. Arterial pressure was reduced by bleeding the animals and raised by transient occlusion of the abdominal aorta. The results indicate that ventilatory responses to chemoreceptor stimulation were augmented by hypotension and depressed by hypertension. In additional studies we excluded the possibility that the findings were produced by a direct effect of changes in arterial pressure on chemoreceptors. Both carotid bifurcations were perfused at constant flow. In one carotid bifurcation, perfusion pressure was raised to stimulate carotid sinus baroreceptors. In the other carotid bifurcation, pressure was constant and nicotine was injected to stimulate carotid chemoreceptors. Stimulation of baroreceptors on one side attenuated the ventilatory response to stimulation of contralateral chemoreceptors. This inhibition was observed before and after bilateral cervical vagotomy. We conclude that there is a major central interaction between baroreceptor and chemoreceptor reflexes so that changes in baroreceptor activity modulate ventilatory responses to chemoreceptor stimulation.

Animals↗
PubMed1981

Responses of aortic chemoreceptors before and after pneumothorax in the cat.

That the response of aortic chemoreceptors to hypercapnia is considerably smaller than that of carotid chemoreceptors is well accepted, but the mechanism for the difference is not known. It has been suggested that surgical exposure of the carotid body may contribute to the difference. Accordingly, the response of aortic body chemoreceptors to CO2 would be expected to resemble quantitatively that of carotid chemoreceptors after exposure of the aortic bodies by pneumothorax. The effect of opening the chest on aortic and carotid chemoreceptor responses to several levels of arterial CO2 and O2 tension and arterial blood pressure were studied in anesthetized cats. The activity of aortic chemoreceptors increased in spite of a decreased stimulus level in the thoracic cavity after pneumothorax. The activity remained higher than the control at all levels of arterial CO2 and O2 tension and arterial blood pressure. However, the slopes of CO2 response curves, which were initially small, did not change after pneumothorax. Thus a change in the normal environment of the aortic bodies by experimental manipulation did not cause the aortic chemoreceptor responses to resemble those of carotid chemoreceptors.

Animals↗
PubMed1983

Opposing effects of dopamine receptor blockade on ventilation and carotid chemoreceptor activity.

To determine the effects of dopamine receptor blockade on the ventilatory responses to hypoxia and hypercapnia we simultaneously measured ventilation and carotid chemoreceptor activity in eight anesthetized cats. During normoxia, haloperidol (1 mg . kg-1 iv) stimulated carotid chemoreceptor activity within 15 s of its administration from a control level of 5.3 +/- 1.1 to 10.4 +/- 2.0 impulses . s-1. Minute ventilation (VI) also rose from 1.00 +/- 0.20 to 1.66 +/- 0.34 l . min-1. Chemoreceptor activity remained elevated, but in the next 15 min VI fell back to or below control levels. Thus haloperidol produced a transient stimulation of ventilation. In the steady state, after haloperidol, carotid chemoreceptor activity was also elevated significantly at all levels of arterial O2 and CO2 partial pressures (PaO2 and PaCO2, respectively). Steady-state ventilation, however, was not significantly different in normoxia (PaO2 82 Torr) after haloperidol despite the elevated chemoreceptor activity. Haloperidol also greatly attenuated the ventilatory response to hypoxia, despite the stimulated carotid chemoreceptor activity. The ventilatory response to hypercapnia was not significantly affected by haloperidol, indicating that its effect was specific for the chemoreflex responses to hypoxia. We conclude that dopamine antagonism by haloperidol blocks the central integration of peripheral chemoreceptor activity, thus attenuating the ventilatory chemoreflex responses to hypoxia while augmenting the carotid chemoreceptor response.

Animals↗
PubMed2004

Peripheral chemoreceptors in health and disease.

Peripheral chemoreceptors (carotid and aortic bodies) detect changes in arterial blood oxygen and initiate reflexes that are important for maintaining homeostasis during hypoxemia. This mini-review summarizes the importance of peripheral chemoreceptor reflexes in various physiological and pathophysiological conditions. Carotid bodies are important for eliciting hypoxic ventilatory stimulation in humans and in experimental animals. In the absence of carotid bodies, compensatory upregulation of aortic bodies as well as other chemoreceptors contributes to the hypoxic ventilatory response. Peripheral chemoreceptors are critical for ventilatory acclimatization at high altitude. They also contribute in part to the exercise-induced hyperventilation, especially with submaximal and heavy exercise. During pregnancy, hypoxic ventilatory sensitivity increases, perhaps due to the actions of estrogen and progesterone on chemoreceptors. Augmented peripheral chemoreceptors have been implicated in early stages of recurrent apneas, congestive heart failure, and certain forms of hypertension. It is likely that chemoreceptors tend to maintain oxygen homeostasis and act as a defense mechanism to prevent the progression of the morbidity associated with these diseases. Experimental models of recurrent apneas, congestive heart failure, and hypertension offer excellent opportunities to unravel the cellular mechanisms associated with altered chemoreceptor function.

Altitude Sickness↗
PubMed1975

Influence of carotid baroreceptors on vascular responses to carotid chemoreceptor stimulation in the dog.

The modification by the carotid baroreceptors of the vascular responses to chemoreceptor stimulation was studied in anesthetized, artificially ventilated, vagotomized dogs. The carotid bifurcations were vascularly isolated and perfused with blood at constant pressures of 134, 215, and 51 mm Hg to cause intermediate, maximal, and minimal inhibition, respectively, of the vasomotor center. At each pressure, stimulation of the carotid chemoreceptors was achieved by perfusion with hypoxic hypercapnic blood. With intermediate inhibition, the chemoreceptor stimulation increased the aortic pressure by 50% and decreased the hind-limb and kidney blood flow (perfusion at constant pressure) by 59% and 19%, respectively. At carotid sinus pressures of 215 and 51 mm Hg, the effects of chemoreceptor stimulation were absent or markedly attenuated. With intermediate sinus pressure, chemoreceptor stimulation decreased the perfusion pressure of the saphenous vein by 27% (perfusion at constant flow). When the sinus pressure was increased to 215 mm Hg, the tone of the vein did not change, but chemoreceptor stimulation was without effect. The present study indicates a central interaction (which may be presynaptic) between the chemoreceptor and baroreceptor inputs such that the vascular responses to chemoreceptor stimulation are inhibited when the carotid sinus activity is maximal or minimal.

Animals↗
PubMed1975

Influence of cardiopulmonary vagal afferent activity on carotid chemoreceptor and baroreceptor reflexes in the dog.

The goal of this study was to determine if physiological levels of cardiopulmonary vagal afferent activity modulate carotid chemoreceptor and baroreceptor reflexes. In anesthetized, ventilated dogs, the aortic nerves and the cervical sympathetic trunks were cut, and atropine was administered so that vagotomy would interrupt only cardiopulmonary afferent impulses. Reflex vascular responses were observed in perfused gracilis muscle and hindpaw. Carotid chemoreceptors were activated with nicotine or hypoxic, hypercapnic blood; carotid baroreceptors were stimulated by changes in carotid pressure. Interruption of vaga afferents augmented reflex vascular responses during changes incarotid pressure from 75 to 125 mm Hg. Interruption of cardiopulmonary vagal afferents potentiated reflex vasoconstrictor (muscle), vasodilator (paw), and vasopressor responses to activation of the carotid chemoreceptors. The potentiation of the chemoreceptor reflex frequently occurred in the absence of increases in base-line vascular resistance. Vagotomy also potentiated ventilatory responses to stimulation of the carotid chemoreceptors in spontaneously breathing dogs. The results indicate that interruption of cardiopulmonary afferents potentiates the vascular and ventilatory responses to activation of the carotid chemoreceptors and augments the gain of the carotid baroreceptor reflex at low carotid pressures. These findings suggest that physiological levels of cardiopulmonary vagal afferent impulses suppress carotid baroreceptor and chemoreceptor reflexes through an interaction in the central nervous system. The suppressive effect on the chemoreceptor reflex may be distinct from tonic restraint of the vasomotor center by vagal afferents, since it involves sympathetic vasodilator as well as vasoconstrictor responses and may occur without suppression of base-line adrenergic constrictor tone.

Afferent Pathways↗
PubMedDate not supplied

Effects of reducing agents on glutathione metabolism and the function of carotid body chemoreceptor cells.

Two current hypotheses of O2 sensing in the carotid body (CB) chemoreceptors suggest participation of oxygen reactive (ROS) species, but they are mechanistically opposed. One postulates that hypoxia decreases ROS levels; the other that hypoxia increases them. Yet, both propose that the ensuing alteration in the cellular redox environment is the key signal triggering hypoxic chemoreception. Since the glutathione redox pair is the main cellular buffer for ROS and the main determinant of the general redox environment of the cells, a way to test whether ROS participate in chemoreception is to determine glutathione levels and to correlate them with the activity of CB chemoreceptor cells. We found that hypoxia does not alter the glutathione reduction potential but that it activates chemoreceptor cell neurosecretion. Incubation of tissues with reduced glutathione increases the glutathione-reducing potential but does not activate chemoreceptor cells in normoxia nor does it modify hypoxic activation. Like reduced glutathione, N-acetylcysteine promoted a general reducing environment in the cells without alteration of chemoreceptor cell activity. N-(mercaptopropionyl)-glycine, like the two previous agents, increases the reduction potential of glutathione. In contrast, the compound activated chemoreceptor cells in normoxia, promoting a dose- and Ca(2+)-dependent neurosecretion and a potentiation of the hypoxic responses. The existence of multiple relationships between glutathione reduction potential in the cells and their activity indicates that the general cellular redox environment is not a factor determining chemoreceptor cell activation. It cannot be excluded that the local redox environments of restricted microdomain(s) in the cells with specific regulating mechanisms are important signals for chemoreceptor cell activity.

Animals↗
PubMedDate not supplied

[Arterial chemoreceptors: cellular and molecular mechanisms in the adaptative and homeostatic function of the carotid body].

The carotid body is a sensory chemoreceptor organ located in the vicinity of the carotid bifurcation. Structurally it is composed of cell clusters formed by chemoreceptor and supporting cells. The sensory nerve endings of the carotid sinus nerve penetrate the clusters to synapse with chemoreceptor cells. The carotid body plays an important role in the control of ventilation during hypoxia, hypercapnia and acidosis. Hypoxia and other natural stimuli are detected by chemoreceptor cells which upon stimulation increase their rate of release of neurotransmitters. Neurotransmitters in turn increase the action potential frequency in the carotid sinus nerve which via its central projections to the brainstem activates ventilation. This review is devoted to the cellular aspects of the function of this chemoreceptor organ. From a brief description of the complex structure of the carotid body, we go to present a summary of the main prevailing theories concerning the transduction mechanisms for hypoxic and acidic/hypercapnic stimuli, with special emphasis on the electrical properties of cultured chemoreceptors cells. A special attention is provided to the possible significance of reactive oxygen species as mediators of the hypoxic transduction cascade. The neurotransmission between chemoreceptor cells and the sensory nerve endings is also covered in certain detail. After a brief historical presentation of the theories of communication between these two structures, we examine, following the classical criteria of neurotransmission, the functional significance of acetylcholine, dopamine, substance P and other neurotransmitters known to be present in chemoreceptor cells.

Adaptation, Biological↗
PubMed1978

Anemia as a stimulus to aortic and carotid chemoreceptors in the cat.

In cats anesthetized with alpha-chloralose, the activities of aortic and carotid chemoreceptor nerves were measured during a control period and during anemia where the hematocrit was lowered in steps by dextran-for-blood exchange. With anemia there was a sustained nonlinear increase in firing of aortic chemoreceptors. There was a greater firing of aortic chemoreceptors for a given lowering of hematocrit from an initial low blood hematocrit than for a similar decrease in hematocrit from an initial high blood hematocrit. Tonic carotid chemoreceptor firing was independent of blood hematocrit and was only transiently increased at the time of dextran-for-blood exchange. The lack of effect of anemia on carotid chemoreceptor activity appeared to be due to sympathetic nerve activity. Section of the sympathetic nerves to the carotid chemoreceptors resulted in an increase in carotid chemoreceptor afferent activity during anemia in a manner similar to the increase in aortic chemoreceptor activity.

Action Potentials↗
PubMed1995

Regulation of sex-specific feeding behavior in fiddler crabs: physiological properties of chemoreceptor neurons in claws and legs of males and females.

This study examined properties of chemoreceptor neurons in the claws and legs of the fiddler crabs Uca pugilator and U. pugnax. The primary goal was to establish the neural basis of previously observed greater female sensitivity to feeding stimulants, and secondarily to compare physiological properties of chemoreceptor neurons in these semi-terrestrial crustaceans with those of fully aquatic forms. Sensitivity of chemoreceptor neurons in claws and legs is sex-specific; individual neurons of females respond to lower stimulus concentrations than male chemoreceptor neurons, and equivalent concentrations elicit greater spiking in female vs male chemoreceptor neurons. Thus, the population of chemoreceptor neurons in females expresses lower thresholds and greater average sensitivity than in males. Greater sensitivity of claw neurons explains observations indicating that females continue to feed at food levels too low to stimulate males. Sensitivity differences in leg neurons of males vs females have no clear behavioral correlate, but suggest that females can orient to more dilute stimuli than males. Chemoreceptor neurons of fiddler crabs have low sensitivities and slow rates of adaptation compared to other crustaceans. Also, neurons in claws adapt less slowly than neurons in legs, which may reflect subtle differences in the chemical stimulus environment experienced by claws vs legs.

Amino Acids↗
PubMed1989

Peripheral chemoreceptor inputs to medullary inspiratory and postinspiratory neurons of cats.

The effect of peripheral chemoreceptor activation on inspiratory and postinspiratory medullary neurons was investigated using intracellular recording techniques. Peripheral chemoreceptors were activated by injecting CO2 saturated 1 N bicarbonate solution into the lingual artery or by electrically stimulating the carotid sinus nerve. Injections of 20-300 microliters bicarbonate solution evoked changes in respiratory frequency and in peak phrenic nerve discharge. The membrane potential of inspiratory alpha neurons, whether bulbospinal or not and independent of their anatomic location, was decreased during inspiration. A sequence of compound excitatory and inhibitory effects were observed when the stimulus was given during the postinspiratory and expiratory phases of the respiratory cycle. Inspiratory beta- and late-inspiratory neurons, however, were inhibited by peripheral chemoreceptor activation. Postinspiratory neurons were strongly activated during postinspiration. Neither class of respiratory neurons were shown to receive direct synaptic inputs from the peripheral chemoreceptors as tested by electrical stimulation of the carotid sinus nerve and signal averaging of the respiratory neuron membrane potential. The experiments revealed differential influences of afferent chemoreceptor activity on various components of the respiratory network. We conclude that chemoreceptor afferents activate non-respiratory modulated medullary neurons which, in turn, activate or inhibit various neurons of the medullary respiratory control network. The responses of each type of respiratory neuron to chemoreceptors afferents may then be considered in the context of this direct interaction as well as the network interactions of the various cells.

Animals↗
PubMed1978

Arterial PO2 and PCO2 stimulus threshold for carotid chemoreceptors and breathing.

The PaO2 and PaCO2 stimulus thresholds for activity of carotid chemoreceptors and for ventilation were investigated in twenty anesthetized adult cats at sea level. Over the range studied PaCO2 threshold for carotid chemoreceptors decreased with increasing intensity of hypoxia showing stimulus interaction. Once begun, the carotid chemoreceptor activity increased gradually at a rate that was inversely related to initial PaO2. The greater the initial hypoxia the greater was the carotid chemoreceptor activity at which the first inspiration occurred, apnea was shorter and inspiratory PaCO2 threshold lower. Hypoxia per se depressed the central mechanism for the resumption of inspiration. We conclude that (1) carotid chemoreceptor PaO2-PaCO2 stimulus thresholds are largely interdependent; (2) these receptors are activated at a lower PaO2-PaCO2 stimulus strength than ventilation is; (3) an increased input from peripheral chemoreceptors initiates breathing at a lower PaCO2 indicating that central chemoreceptor threshold is lower than the PCO2 threshold for inspiration; (4) a finite total input from the receptors is needed to start ventilation.

Animals↗
PubMed1981

Augmentation of carotid body chemoreceptor responses by isoproterenol in the cat.

The effects of intravenous injections of isoproterenol (0.5-2 microgram) on the responses of carotid body chemoreceptor afferents and on integrated phrenic activity were investigated in twelve anesthetized and three decerebrate, unanesthetized cats. All animals were paralyzed and artificially ventilated. Isoproterenol stimulated carotid chemoreceptor activity and this stimulation was augmented by both hypoxia and hypercapnia. Following an injection of isoproterenol, the ratio of the minute phrenic activity relative to mean carotid chemoreceptor activity was increased. Thus, the stimulation of inspiratory phrenic output exceeded the stimulation of the chemoreceptor afferent input, and the peripheral chemoreflex activity does not account for the entire ventilatory response. To distinguish between a direct effect of isoproterenol and a possible secondary effect mediated via an increased venous return and an increased PaCO2, the latencies of the response of carotid chemoreceptors to both isoproterenol and hypercapnia were compared before and after carbonic anhydrase inhibition by acetazolamide. After acetazolamide, the latency of the response to hypercapnia increased from 3.5 sec to 8 sec whereas the latency of response to isoproterenol increased less, from 4.7 sec to 6.3 sec. Thus, isoproterenol stimulation was not mediated by CO2-H+. Propanolol, which blocked the systemic vascular effect, only partially blocked the chemoreceptor stimulation caused by isoproterenol, indicting that the effect of isoproterenol on chemoreceptor activity was not due to systemic cardiovascular changes.

Acetazolamide↗
PubMed1988

Chemoreceptor stimulation interferes with regional hypoxic pulmonary vasoconstriction.

Hypoxemia interferes with the diversion of blood flow away from hypoxic regions of the lung, possibly through activation of the arterial chemoreceptor reflex. The purpose of this study was to determine if selective stimulation of carotid chemoreceptors reduces the diversion of flow (hypoxic vasoconstriction) when normal systemic oxygen levels are present. Chloralose anesthetized dogs were paralyzed and each lung was separately ventilated via a dual-lumen endobronchial tube. Left pulmonary artery (QL) and main pulmonary artery (QT) blood flows were measured with electromagnetic flow probes. Chemoreceptors were stimulated by perfusion of the carotid sinuses with hypoxic, hypercapnic blood. QL/QT averaged 46 +/- 4, 29 +/- 2, and 36 +/- 4% during bilateral O2 ventilation (control), left lung N2 ventilation, and left lung N2 plus chemoreceptor stimulation in dogs treated with the cyclo-oxygenase inhibitor meclofenamate. After vagotomy, QL/QT averaged 45 +/- 4, 27 +/- 3, and 28 +/- 2% during the same conditions. QL/QT decreased significantly from control (P less than 0.05) during left lung N2 alone but did not decrease during left lung N2 plus chemoreceptor stimulation in dogs with intact vagi. In contrast, QL/QT decreased significantly both before and during chemoreceptor stimulation in vagotomized dogs. The same responses were observed in dogs not treated with meclofenamate. These results indicate that selective stimulation of arterial chemoreceptors can interfere with regional hypoxic vasoconstriction and suggest that the vagus nerves may mediate this effect.

Animals↗
PubMed1991

Sympathetic influence on carotid chemoreceptor response to substance P in the cat.

Previous studies have suggested that substance P (SP) may play a role in the carotid chemoreceptor response to hypoxia. Given the data from these studies we speculated that within the carotid body hypoxia might release SP which then acts on the chemosensitive unit. Concomitantly SP might be released in the superior cervical ganglion (SCG) and increase sympathetic outflow to the carotid body by interacting with acetylcholine in the SCG. The resulting vasoconstriction in the carotid body would further increase neural output from the carotid body. Hence we hypothesized that the exogenous SP on the carotid chemoreceptor neural activity would decrease after eliminating preganglionic inflow into the SCG. The hypothesis was tested using anesthetized, paralyzed and artificially ventilated cats. Neural activity from the carotid body (carotid chemoreceptor activity) or from the SCG (ganglioglomerular efferent nerve activity (GGN)) was measured. Close intra-arterial administration of SP (10 micrograms) caused a sustained stimulation of the carotid chemoreceptor activity which was accompanied by a fall in arterial blood pressure. The magnitude and time-course of the carotid body responses were extremely variable among the cats. The duration of increased chemoreceptor activity was significantly shortened after a transection of the cervical sympathetic nerve (CVSN). As a control, the duration of carotid body stimulation produced by the second injection of SP in a group of sham-operated cats was measured. This was essentially the same as the first injection, suggesting that the tachyphylactic effect of SP was negligible. The effects of the commonly used pharmacological agents (nicotine, cyanide, dopamine) on carotid chemoreceptor activity were not affected by the transection of the CVSN, GGN activity was also increased by exogenous SP. These results suggest that the effect of exogenous SP on carotid chemoreceptor activity consists of two components: (1) an initial direct excitatory effect; (2) a slowly developing excitatory effect mediated by the sympathetic outflow to the carotid body. The effects could be augmented by the accompanying hypotension.

Animals↗
PubMed1992

Effect of chemoreceptor stimulation on the periodicity of renal sympathetic nerve activity in anesthetized cats.

The effect of chemoreceptor stimulation, with asphyxia (1 min), hypoxia (2 min) or hypercapnia (2 min), on the periodicity of synchronized renal sympathetic nerve activity (RNA) was examined in anesthetized cats before and after peripheral chemoreceptor and baroreceptor denervation. RNA was filtered between 50-3000 Hz, rectified and integrated. Time intervals, less than 500 ms, between synchronized interburst intervals were measured and used to produce periodicity histograms. Under control normoxia two major periodicities were evident, a Tc rhythm between 6 and 17 c/s comprising 34 +/- 5% (+/- SE) of measured intervals and a Tb rhythm between 2 and 6 c/s with a 66% probability. The mean periods of Tc and Tb were 110 +/- 6 ms and 299 +/- 7 ms respectively. The periodicity distribution and mean Tc and Tb rhythms for RNA discharge under various chemoreceptor stimulations were not significantly changed despite significant increases in arterial blood pressure in all cases. The amplitude and overall number of synchronized RNA peaks were however increased with chemoreceptor stimulation. When asphyxia was applied under a constant arterial pressure the periodicity of synchronized RNA still was not significantly altered. Baroreceptor and peripheral chemoreceptor denervation led to an increase in the probability of the Tc mode and reduction in the Tb mode, once again the application of chemoreceptor stimulation did not significantly alter the frequency distribution of synchronized RNA. The results indicate that chemoreceptor stimulation does not affect the 10 c/s fundamental rhythm and the stability of gate operators altering Tc/Tb proportions, although it can alter the number of active fibres and interacts with the baroreflexes to maintain RNA at elevated blood pressures. The results support our model that the Tc mode reflects a fundamental periodicity of central origin and the Tb mode a periodicity of cardiac related RNA, which is produced by the opening and closing of gate operators to the fundamental rhythm.

Anesthesia↗
PubMed1995

Nitric oxide mediates chemoreceptor inhibition in the cat carotid body.

Numerous studies have demonstrated that carotid sinus nerve fibers mediate a so-called "efferent" inhibition of carotid body chemoreceptors. However, the mechanism(s) underlying this phenomenon are not understood. Recently, it has been shown that an extensive plexus of nitric oxide synthase-containing carotid sinus nerve fibers innervate the carotid body, and that many fine, beaded fibers can be seen in close proximity to small blood vessels as well as lobules of parenchymal cells. The present study examined the effects of centrifugal neural activity in the carotid sinus nerve on the accumulation of [3H]citrulline synthesized from [3H]arginine in the cat carotid body, and the possible involvement of nitric oxide in mediating "efferent" chemoreceptor inhibition. Electrical stimulation of carotid sinus nerve C-fibers evoked an increase in [3H]citrulline accumulation in the carotid body, which was Ca(2+)-dependent and blocked by L-NG-nitroarginine methylester (0.1 mM), an inhibitor of nitric oxide synthase. Using a vascularly perfused in vitro carotid body preparation, chemoreceptor activity was recorded from thin nerve filaments split-off from the main trunk of the carotid sinus nerve. Electrical stimulation of the main nerve trunk at C-fiber intensities inhibited steady-state chemoreceptor discharge, and this effect was blocked by L-NG-nitroarginine methylester. However, when the organ preparation was switched to the superfuse-only mode, carotid sinus nerve stimulation failed to alter the steady-state discharge, but under these conditions, prolonged nerve stimulation (> 5 min) did attenuate the chemoreceptor response to hypoxia, an effect which was likewise blocked by L-NG-nitroarginine methylester. The present data, together with previous anatomical findings that nitric oxide synthase immunoreactivity is present in both sensory and autonomic ganglion cells innervating the carotid body, suggest that two neural mechanisms may be involved in the inhibitory neural regulation of carotid chemoreceptors. One mechanism appears to involve nitric oxide release from intralobular sensory C-fibers, which lie in close proximity to the chemoreceptor type I cells. The other mechanism involves release of nitric oxide from perivascular terminals of autonomic microganglia neurons, which control carotid body blood flow.

Animals↗