Carotid Baro Research Articles

Vagal baro- and chemoreceptors in middle internal carotid artery and carotid body in rat.

The glossopharyngeal nerve, via the carotid sinus nerve (CSN), presents baroreceptors from the internal carotid artery (ICA) and chemoreceptors from the carotid body. Although neurons in the nodose ganglion were labelled after injecting tracer into the carotid body, the vagal pathway to these baro- and chemoreceptors has not been identified. Neither has the glossopharyngeal intracranial afferent/sensory pathway that connects to the brainstem been defined. We investigated both of these issues in male Sprague-Dawley rats (n=40) by injecting neural tracer wheat germ agglutinin-horseradish peroxidase into: (i) the peripheral glossopharyngeal or vagal nerve trunk with or without the intracranial glossopharyngeal rootlet being rhizotomized; or (ii) the nucleus of the solitary tract right after dorsal and ventral intracranial glossopharyngeal rootlets were dissected. By examining whole-mount tissues and brainstem sections, we verified that only the most rostral rootlet connects to the glossopharyngeal nerve and usually four caudal rootlets connect to the vagus nerve. Furthermore, vagal branches may: (i) join the CSN originating from the pharyngeal nerve base, caudal nodose ganglion, and rostral or caudal superior laryngeal nerve; or (ii) connect directly to nerve endings in the middle segment of the ICA or to chemoreceptors in the carotid body. The aortic depressor nerve always presents and bifurcates from either the rostral or the caudal part of the superior laryngeal nerve. The vagus nerve seemingly provides redundant carotid baro- and chemoreceptors to work with the glossopharyngeal nerve. These innervations confer more extensive roles on the vagus nerve in regulating body energy that is supplied by the cardiovascular, pulmonary and digestive systems.

Role of Chemoreceptor Activation in Hemodynamic Responses to Electrical Stimulation of the Carotid Sinus in Conscious Rats.

Electric carotid baroreflex activation has been used to treat patients with resistant hypertension. It is hypothesized that, in conscious rats, combined activation of carotid baro- and chemoreceptors afferences attenuates the reflex hypotension. Rats were divided into 4 groups: (1) control group, with unilateral denervation of the right carotid chemoreceptors; (2) chemoreceptor denervation group, with bilateral ligation of the carotid body artery; (3) baroreceptor denervation group, with unilateral denervation of the left carotid baroreceptors and right carotid chemoreceptors; and (4) carotid bifurcation denervation group, with denervation of the left carotid baroreceptors and chemoreceptors, plus denervation of the right carotid chemoreceptors. Animals were subjected to 4 rounds of electric stimulation (5 V, 1 ms), with 15, 30, 60, and 90 Hz applied randomly for 20 s. Electric stimulation caused greater hypotensive responses in the chemoreceptor denervation group than in the control group, at 60 Hz (-37 versus -19 mm Hg) and 90 Hz (-33 versus -19 mm Hg). The baroreceptor denervation group showed hypertensive responses at all frequencies of stimulation. In contrast, the carotid sinus denervation group showed no hemodynamic responses. The control group presented no changes in heart rate, whereas the chemoreceptor denervation group and the baroreceptor denervation group showed bradycardic responses. These data demonstrate that carotid chemoreceptor activation attenuates the reflex hypotension caused by combined electric stimulation of the carotid sinus and the carotid sinus nerve in conscious rats. These findings may provide useful insight for clinical studies using baroreflex activation therapy in resistant hypertension and heart failure.

Modulation of emetic response by carotid baro- and chemoreceptor activations

We hypothesized that baroreceptor or chemoreceptor activation might be involved in the emetic, and prodromal cardiovascular and respiratory responses. To test this hypothesis, we induced the emetic responses by gastric distension in anesthetized Suncus murinus (house musk shrew), that had intact and absent baroreceptor and chemoreceptor afferents. Secondly, we stimulated the aortic depressor nerve (ADN) and the carotid sinus nerve (CSN) with or without gastric distension. Internal carotid artery ligation in the bifurcation area, which abolished reflex bradycardia by baroreceptor activation, and abolition of chemoreceptor reflex bradycardia and hyperventilation, by carotid body denervation, suppressed the emetic response but did not abolish it. ADN denervation, which produced no significant effects on the baroreceptor or chemoreceptor reflex bradycardia, had no effect on the emetic response, including the prodromal phase. CSN stimulation with gastric distension elicited retching accompanied by reflex bradycardia and hypotension during or just after stimulation, whereas ADN stimulation with gastric distension did not induce the cardiovascular reflex, and had no effects on the emetic response. These results indicate that carotid, rather than aortic, baroreceptor or chemoreceptor activation plays an important role in the augmentation of cardiac parasympathetic activity and the development of emetic response. In conclusion, carotid baroreceptor or chemoreceptor activation, which is non-emetic stimulation, acts as a modulator in the central mechanisms of emesis.

Hyperglycemic response to hemorrhage is modulated by baroreceptors unloading but not by peripheral chemoreceptors activation

The aim of this study was to assess the relative participation of carotid baro- and chemoreceptors on plasma glucose and lactate level in response to hemorrhagic hypotension. We also evaluated the effects of selective activation of carotid chemoreceptors. One week before the experiments, male Wistar rats (250–300 g) were submitted to bilateral total carotid denervation (BCD-group), or to bilateral ligature of the carotid body artery (ChD-group). During the same surgical procedure, a chronic jugular catheter for blood sampling and hemorrhage (1.2 mL/100 g/2 min) and polyethylene cannula was inserted into the left femoral artery for cardiovascular monitoring. One group submitted to fictitious surgery was used as a surgical control (Sham-group). Carotid chemoreceptors were selectively activated by sodium cyanide (NaCN, 40 μg/0.1 mL i.v.) in the Sham and ChD group. The results showed that hyperglycemic response to hemorrhage in the BCD-group was reduced whereas in the ChD-group there was no significant change in this parameter compared to the Sham group (8.6 ± 0.5 mM, Sham-hemorrhaged, n = 8; 7.2 ± 0.3 mM, BCD-hemorrhaged, n = 8 and 9.4 ± 0.6 mM, ChD, n = 8, p < 0.05). Increased plasma lactate levels following hemorrhage were observed in all the three experimental groups throughout the experimental period and there were no differences between the groups. Chemoreceptor stimulation by NaCN also produced hyperglycemia, as well as an increase in blood pressure and bradycardia but did not affect plasma lactate concentration. Ligature of the carotid body artery annulled the cardiovascular responses induced by NaCN, but did not change the hyperglycemic response to hypoxia. In conclusion, our data indicate that carotid chemoreceptors do not play any major role in overall metabolic response to hypoxia or hemorrhagic hypotension. Furthermore, the results suggest that carotid baroreceptors unloading play a predominant role as main source of afferent impulses leading to the hyperglycemic response to hemorrhage. In addition our data shows that the metabolic response and cardiovascular adjustment to hypoxia can be dissociated by ligature of the carotid body artery.

Denervation of carotid baro- and chemoreceptors in humans.

Experimental denervation in animals has shown that carotid baro- and chemoreceptors play an eminent role in maintaining blood pressure and blood gas homeostasis. Denervation of carotid sinus baro- and chemoreceptors in humans may occur as a complication of invasive interventions on the neck or after experimental surgical treatment in asthma. In this topical review, the short- and long-term effects of carotid baro- and chemoreceptor denervation on the control of circulation and ventilation in humans are discussed. Carotid baroreceptor denervation in humans causes a persistent decrease in vagal and sympathetic baroreflex sensitivity and an increase in blood pressure variability; however, carotid denervation does not lead to chronic hypertension. Therefore, although carotid baroreceptors contribute to short-term blood pressure control, other receptors are able to maintain normal chronic blood pressure levels in the absence of carotid baroreceptors. Conversely, carotid chemoreceptor denervation leads to permanent abolition of normocapnic ventilatory responses to hypoxia and reduced ventilatory responses to hypercapnia.

Ventricular volume elasticity: a component of cardiovascular control?

According to Koepchen, stimulation of different receptors within a complex network produces typical patterns of effector responses. We investigated whether the dynamical volume elasticity of the heart chamber is an independent component of cardiovascular control. The measurement of the dynamical volume elasticity was calculated by changes of the eigenfrequency of a modified catheter transducer system. The carotid baro- and chemoreflex affected end-diastolic pressure, contractility and calculated diastolic and systolic elasticity to different extents. In conclusion, cardiac volume elasticity is an independent element interacting with other parameters in cardiovascular control.

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

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

Distribution of fos proteins in petrosal ganglion cells following carotid baro- and chemo-receptor stimulation

Distribution of fos proteins in petrosal ganglion cells following carotid baro- and chemo-receptor stimulation

Three types of neurochemically defined autonomic fibres innervate the carotid baroreceptor and chemoreceptor regions in the guinea-pig

The innervation of the carotid body, carotid sinus, and neighbouring arteries (common carotid artery; external carotid artery; occipital artery; ascending pharyngeal artery) was investigated in guinea-pigs by means of glyoxylic acid-induced catecholamine-fluorescence and immunohistochemistry using a variety of antisera against neuropeptides and tyrosine hydroxylase (TH). Fibres displaying catecholamine-fluorescence, TH- and neuropeptide Y-like immunoreactivity (NPY-LI) were less numerous in the carotid sinus than in all other arterial segments. Vasoactive intestinal polypeptide (VIP)-LI axons were almost lacking in the common carotid, external carotid and occipital arteries, consistently found in the carotid sinus, and more numerous in the ascending pharyngeal artery. Catecholaminergic, TH-, NPY- and VIP-LI fibres were observed deep in the media of the carotid sinus, where the baroreceptor terminals are located. In contrast, they did not enter the media in the adjacent arterial segments. All these fibres disappeared following excision of the superior cervical ganglion, but were unaffected by combined transection of the carotid sinus nerve and resection of the no-dose ganglion, suggesting a sympathetic origin. Double-staining immunofluorescence revealed at least three types of autonomic, presumably sympathetic fibres in the carotid sinus: 1) TH+/NPY+, 2) NPY+/VIP+, and 3) VIP+ fibres. This points to a non-noradrenergic efferent innervation of the carotid sinus in addition to the hitherto known noradrenergic sympathetic fibres. The three populations of autonomic fibres seen in the carotid sinus were also observed in the carotid body, but the paucity of NPY+/VIP+ double-labelled fibres raises doubt as to the functional significance of this particular fibre type in modulating arterial chemoreception. The multiplicity of neurochemically defined autonomic nerves to the carotid baro- and chemoreceptor regions probably reflects functionally separate pathways that are differently regulated and exert different effects.

Units in the amygdala responding to activation of carotid baro- and chemoreceptors.

The distribution of units in the amygdala responding to selective activation of baro- and chemoreceptors was investigated in 12 cats under alpha-chloralose anesthesia. Changes in the firing frequency of spontaneously discharging units were monitored during baroreceptor activation (BA) (phenylephrine hydrochloride, 2 micrograms/kg iv) and chemoreceptor activation (CA) (sodium cyanide, 25 micrograms in 0.1 ml saline into the medial thyroid artery). CA altered the firing frequency of 23% (35/154) of the units; 37% (13/35) were excited, and 63% (22/35) were inhibited. BA altered the firing frequency of 16% (24/154) of the units; 71% (17/24) were excited, while 29% (7/24) were inhibited. The units responsive to CA were located primarily in the dorsomedial amygdala, while those responsive to BA were located primarily in the ventrolateral amygdala. The anatomic separation of units within the amygdala responding to activation of baroreceptors or chemoreceptors suggests that the specificity of function of different parts of the amygdala is related to the different kinds of inputs received by these components of the amygdala from cardiovascular receptors.

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

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

Comparison of the averaged nervous activities of aortic and carotid sinus nerves.

ARTICLESComparison of the averaged nervous activities of aortic and carotid sinus nervesH Irisawa, and I NinomiyaH Irisawa, and I NinomiyaPublished Online:01 Aug 1967https://doi.org/10.1152/ajplegacy.1967.213.2.504MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByDischarges of aortic and carotid sinus baroreceptors during spontaneous motor activity and pharmacologically evoked pressor interventions11 May 2014 | The Journal of Physiological Sciences, Vol. 64, No. 4Signal transduction of aortic and carotid sinus baroreceptors is not modified by central command during spontaneous motor activity in decerebrate catsKanji Matsukawa, Kei Ishii, Akito Kadowaki, Tomoko Ishida, Mitsuhiro Idesako, and Nan Liang15 May 2014 | American Journal of Physiology-Regulatory, Integrative and Comparative Physiology, Vol. 306, No. 10Modulation of emetic response by carotid baro- and chemoreceptor activationsAutonomic Neuroscience, Vol. 128, No. 1-2Effects of the Head-Down Tilt Posture on Postnatal Development of the Aortic Baroreflex in the Rabbit.The Japanese Journal of Physiology, Vol. 52, No. 2Comparison of aortic and carotid baroreflex stimulus–response characteristics in humansAutonomic Neuroscience, Vol. 88, No. 1-2Cardiovascular responses to time delays of electrocardiogram-coupled electrical stimulation of carotid sinus nerves in dogsJournal of the Autonomic Nervous System, Vol. 25, No. 2-3An Analyzer for Autonomic Nerve Activities in Acute and Chronic AnimalsIEEE Transactions on Biomedical Engineering, Vol. BME-33, No. 1Baroreflex Control of Systemic Arterial Pressure and Vascular Bed1 January 2011Chronic localized hypotension and resetting of carotid sinus baroreceptors. Electrophysiological and histological studies in the dog.Circulation Research, Vol. 49, No. 3Coarctation of the aorta and baroreceptor resetting. A study of carotid baroreceptor stimulus-response characteristics before and after surgical repair in the dog.Circulation Research, Vol. 48, No. 3Cardiovascular neurography: Cardiac-rhythm based neurosignal distribution displayMedical & Biological Engineering & Computing, Vol. 18, No. 1Hypertension following denervation of aortic baroreceptors in unanesthetized dogs.Circulation Research, Vol. 45, No. 1Effect of Changing the Frequency of Conditioning Tetanus on Depressor Responses Evoked by Stimulation of the Aortic Nerve26 September 2008 | Archives Internationales de Physiologie et de Biochimie, Vol. 86, No. 4Response Characteristics of Carotid Baroreceptors to Steady PressureAn inexpensive technique for analysis of aortic-nerve activityMedical & Biological Engineering, Vol. 11, No. 5Comparison of Afferent Activity of Canine Aortic and Sinus NervesCirculation Research, Vol. 31, No. 4Reflex Effects of Stimulation of Carotid Sinus and Aortic Baroreceptors on Hindlimb Vascular Resistance in DogsCirculation Research, Vol. 29, No. 2The Effect of Section of Aortic nerves on the Relationship Between the Resting Blood Pressure and Magnitude of Pressure Responses in the Rabbit27 September 2008 | Archives Internationales de Physiologie et de Biochimie, Vol. 78, No. 1 More from this issue > Volume 213Issue 2August 1967Pages 504-510 Copyright & PermissionsCopyright © 1967 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1967.213.2.504PubMed6036338History Published online 1 August 1967 Published in print 1 August 1967 Metrics

On the mechanism for bradycardia induced by acute systemic anoxia in the dog.

The effects of acute systemic anoxia on heart rate were investigated in 46 anaesthetized, artificially ventilated and spontaneously breathing dogs. Severe anoxia produced by inhalation of 100 per cent nitrogen over a period of 1 to 3 min elicited in both groups of animals a biphasic response consisting of a primary tachycardia and secondary bradycardia. Whereas primary tachycardia was usually moderate, secondary bradycardia was very pronounced and amounted to a 45.8 per cent reduction of heart rate in artificially ventilated dogs, and to 67.2 per cent in dogs breathing spontaneously. Bilateral cervical vagotomy, atropinization and ganglionic blockade caused consistently a considerable reduction or abolition of anoxic bracycardia. On the contrary, elimination of the sympatho-adrenal system by means of spinal cord destruction and bilateral adrenalectomy was conducive to an evident enhancement of bradycardia. The intensity of bradycardia was not reduced following denervation of carotid and aortic baro- and chemoreceptors. On the contrary, denervation invariably resulted in a considerable increase of bradycardia. It is concluded that secondary anoxic bradycardia is mainly due to the increased tone of the vagal cardioinhibitory center, the local depressant action of anoxia on the heart itself being of minor importance. Increased vagal tone is opposed by the concomitant stimulation of the sympatho-adrenal system. Anoxic bradycardia cannot be regarded as resulting from stimulation of carotid and aortic receptors. It is, therefore, inferred that some other mechanism, reflex or central, is activated during acute systemic anoxia giving rise to the increased vagal discharge to the heart.