Carotid Body Stimulation Research Articles

Chronic CO inhalation and carotid body catecholamines: testing of hypotheses.

The purpose of this study was twofold: one concerns carotid blood flow and tissue PO2 and the other the effect of chronic hypoxic hypoxia on enhanced catecholamine content. The rationale was that chronic CO inhalation would not mimic the effect of hypoxia on the carotid body if its tissue blood flow is sufficiently high to counteract the effect of CO on O2 delivery and, hence, on tissue PO2. The differential effects of CO on the carotid body and erythropoietin-producing tissue would also indicate that the effect of hypoxic hypoxia on the carotid body is the result of a direct action of a local low O2 stimulus rather than secondary to a systemic effect initiated by other O2-sensing tissues. To test these alternatives we studied the effects of chronic CO inhalation on carotid body catecholamine content and hematocrit in the rats, which were exposed to an inspired PCO of 0.4-0.5 Torr at an inspired PO2 of approximately 150 Torr for 22 days. The hematocrit of CO-exposed rats was 75 +/- 1.1% compared with 48 +/- 0.7% in controls. Dopamine and norepinephrine content of the carotid bodies (per pair) was 5.88 +/- 0.91 and 3.02 +/- 0.19 ng, respectively, in the CO-exposed rats compared with 6.20 +/- 1.0 and 3.29 +/- 0.6 ng, respectively, in the controls. Protein content of the carotid bodies (per pair) was 18.4 +/- 1.6 and 20.5 +/- 0.9 micrograms, respectively. Thus, despite a vigorous erythropoietic response, the CO-exposed rats failed to show any significant stimulation of carotid body in terms of the content of either catecholamine or protein. The results suggest that carotid body tissue PO2 is not compromised by moderate carboxyhemoglobinemia because of its high tissue blood flow and that the chronic effect of hypoxic hypoxia on carotid body is direct.

Differential responses of expiratory muscles to chemical stimuli in awake dogs

We assessed respiratory muscle response patterns to chemoreceptor stimuli (hypercapnia, hypoxia, normocapnic hypoxia, almitrine, and almitrine + CO2) in six awake dogs. Mean electromyogram (EMG) activities were measured in the crural (CR) diaphragm, triangularis sterni (TS), and transversus abdominis (TA). Hypercapnia and normocapnic hypoxia caused mild to marked hyperpnea [2-5 times control inspiratory flow (VI)] and increased activity in CR diaphragm, TS, and TA. When hypocapnia was permitted to develop during hypoxia and almitrine-induced moderate hyperpnea, CR diaphragm activity increased, whereas TS and TA activities usually did not change or were reduced below control. Over time in hypercapnia, CR diaphragm, TS, and TA were augmented and maintained at these levels over many minutes; with hypoxic hyperventilation CR diaphragm, TS, and TA were first augmented but then CR diaphragm remained augmented while TS and, less consistently, TA were inhibited over time. Marked hyperpnea (4-5 times control) due to carotid body stimulation increased TA and TS EMG activity despite an accompanying hypocapnia. We conclude that in the intact awake dog 1) carotid body stimulation augments the activity of both inspiratory and expiratory muscles; 2) hypocapnia overrides the augmenting effect of carotid body stimulation on expiratory muscles during moderate hyperpnea, usually resulting in either no change or inhibition; 3) at higher levels of hyperpnea both chemoreceptor stimulation and stimulatory effects secondary to a high ventilatory output favor expiratory muscle activation; these effects override any inhibitory effects of a coincident hypocapnia; and 4) expiratory muscles of the rib cage/abdomen may be augmented/inhibited independently of one another.

Brain hypoxia preferentially stimulates genioglossal EMG responses to CO2

Although the dominant respiratory response to hypoxia is stimulation of breathing via the peripheral chemoreflex, brain hypoxia may inhibit respiration. We studied the effects of two levels of brain hypoxia without carotid body stimulation, produced by inhalation of CO, on ventilatory (VI) and genioglossal (EMGgg) and diaphragmatic (EMGdi) responses to CO2 rebreathing in awake, unanesthetized goats. Neither delta VI/delta PCO2 nor VI at a PCO2 of 60 Torr was significantly different between the three conditions studied (0%, 25%, and 50% carboxyhemoglobin, HbCO). There were also no significant changes in delta EMGdi/delta PCO2 or EMGdi at a PCO2 of 60 Torr during progressive brain hypoxia. In contrast, delta EMGgg/delta PCO2 and EMGgg at a PCO2 of 60 Torr were significantly increased at 50% HbCO compared with either normoxia or 25% HbCO (P less than 0.05). The PCO2 threshold at which inspiratory EMGgg appeared was also decreased at 50% HbCO (45.6 +/- 2.6 Torr) compared with normoxia (55.0 +/- 1.4 Torr, P less than 0.02) or 25% HbCO (53.4 +/- 1.6 Torr, P less than 0.02). We conclude that moderate brain hypoxia (50% HbCO) in awake, unanesthetized animals results in disproportionate augmentation of EMGgg relative to EMGdi during CO2 rebreathing. This finding is most likely due to hypoxic cortical depression with consequent withdrawal of tonic inhibition of hypoglossal inspiratory activity.

Carotid body control of bronchial circulation in sheep.

The bronchial vascular response to chemoreceptor stimulation was studied in sheep anesthetized with alpha-chloralose, paralyzed with pancuronium, and artificially ventilated with room air. Blood flow through the common bronchial artery was measured with an electromagnetic flow-meter. Pressures were measured in the left atrium and aorta using appropriately placed catheters connected to pressure transducers. The carotid body was vascularly isolated and perfused at aortic pressure with blood of varied PO2 and PCO2. The viability of our preparation was assessed by the occurrence of a bradycardia in response to carotid body stimulation, and only data from animals demonstrating a bradycardia were analyzed. During hypoxic perfusion of the carotid body, heart rate decreased 6% (P less than 0.05). Bronchial blood flow increased by 46% and bronchial vascular resistance decreased by 23%, both of which were significant changes (P less than 0.05). During control experiments in which the carotid body was perfused with normoxic blood, there were no significant (P greater than 0.05) changes in any of the parameters. These data suggest that carotid body stimulation results in a reflex bronchial vasodilation.

Cooling the intermediate area of the ventral medullary surface affects tracheal responses to hypoxia

The intermediate area of the ventral medullary surface (VMS) influences changes in airway tone caused by hypercapnia and intrapulmonary irritant receptor activation. These studies evaluated the effects of cooling the intermediate area of the VMS on the reflex hypoxic responses of the trachealis smooth muscle and of the phrenic nerve. Anesthetized, paralyzed cats were hyperventilated with 100% oxygen to produce phrenic neural apnea. Tracheal tone was measured indirectly by evaluating pressure changes in an innervated tracheal segment and the phrenic electroneurogram was determined from the central end of a cut cervical root. Switching the inspired gas to 12% O 2 increased tracheal pressure of 11 of 12 cats but caused phrenic activity to reappear in only 6 of the animals. Ventilation with 6% O 2 significantly increased tracheal constriction prior to phrenic activity. After intravenous administration of atropine methyl nitrate tracheal responses to hypoxia were abolished but phrenic neural responses were unaltered. Neither the tracheal pressure not the phasic phrenic electroneurogram responded to hypoxia after cutting the carotid sinus nerves. When the intermediate area of the VMS was cooled to 20°C prior to ventilation with the hypoxic gases, both tracheal and phrenic responses were significantly diminished. While the cats were hyperventilated with 6% O 2, cooling of the intermediate area significantly diminished tracheal pressure and phrenic nerve activity and both returned to the same levels after rewarming. Cooling of the intermediate area blunted tracheal and phrenic responses to carotid body stimulation by NaCN. However, the appearance of tracheal constriction prior to the onset of phasic phrenic activity may suggest that increased trachealis tone may occur independent of cyclical respiratory activity.

Carotid body hypercapnia does not elicit ventilatory acclimatization in goats

The carotid body (CB) perfusion model utilizes surgical vascular ligations to allow isolated blood supply to a single in situ CB in awake goats. The contralateral CB was excised. By use of an extracorporeal pump-oxygenator system the blood gas composition perfusing the CB can be controlled independently from that of the systematic arterial system including the brain. Using this model we compared the responses of systemically normoxic goats to CB hypercapnia and CB hypoxia. In 6 goats CB sitmulation with hypercapnic-normoxic blood (mean Pcb CO 2 = 78Torr, mean Pcb O 2 ≅ 100 Toor) produced acute hyperventillation (mean decrease in Pa CO 2 of 5.2 Torr, P < 0.05) which remained constant over the 4-h perfusion period, Lack of a progressively increasing hyperventilation indicates that ventilatory acclimatization did not occur with hypercapnic CB perfusion. Hypoxic-normocapnic CB stimulation (mean Pcb O 2 = 40 Torr, mean PcB CO 2 = 39 Torr) produced an acute mean in Pa CO 2 of 5.5 Torr ( P < 0.05) in 6 additional goats. In contrast to CB hypercapina, the acute hyperventilation induced by CB hypoxia was followed by a progressive time-dependent additional mean decrease in Pa CO 2 of 5.6 Torr ( P < 0.05) over a 4-h period (ventilatory acclimatization). These data are compatible with the concept of separate mechanisms for hypercapnia and hypoxia in the CB suggest that the early phase of ventillatory acclimatization to hypoxia in goats may result from a time-dependent increase in CB afferent output.

Ventilatory acclimatization to hypoxia is not dependent on cerebral hypocapnic alkalosis.

We previously demonstrated that, in awake goats, 6 h of hypoxic carotid body perfusion during systemic normoxia produced time-dependent hyperventilation that is typical of ventilatory acclimatization to hypoxia (VAH). The hypocapnic alkalosis that occurred could have produced VAH by inducing cerebral vasoconstriction and brain lactic acidosis even though systemic arterial normoxia was maintained. In the present study we tested the hypothesis that hypocapnic alkalosis is a necessary component of VAH. Goats were prepared so that one carotid body could be perfused, from an extracorporeal circuit, with blood in which gas tensions could be controlled independently from the blood perfusing the systemic arterial system, including the brain. Using this preparation we carried out 4 h of hypoxic carotid body perfusion while maintaining systemic arterial (and brain) normoxia in awake goats. Expired minute ventilation (VE) was measured while CO2 was added to inspired air to maintain normocapnia. Carotid body PCO2 and PO2 were maintained near 40 Torr during the 4-h carotid body perfusion. Control mean VE was 8.65 +/- 0.48 l/min (mean +/- SE). With acute carotid body hypoxia (30 min) VE increased to 21.73 +/- 2.02 l/min (P less than 0.05); over the ensuing 3.5 h of carotid body hypoxia, VE progressively increased to 39.14 +/- 4.14 l/min (P less than 0.05). These data indicate that neither cerebral hypoxia nor hypocapnic alkalosis are required to produce VAH. After termination of the 4-h carotid body stimulation, hyperventilation was not maintained in these studies, i.e., there was no deacclimatization. This suggests that acclimatization and deacclimatization are produced by different mechanisms.

Evidence that the arterial baroreceptors influence muscle blood flow and not subcutaneous flow in man.

Studies in man indicate that skeletal muscle blood flow is modulated via high pressure baroreceptors located in the carotid body. However, whether subcutaneous blood flow is influenced in this way remains controversial. Therefore, the aim of the present study was to determine whether subcutaneous as well as skeletal muscle blood flow was influenced by direct carotid body stimulation; this was done by means of neck suction. Six young healthy males were investigated. Subcutaneous and skeletal muscle blood flow in the forearm was measured by the local 133Xe washout technique. Neck suction of -20 mmHg was applied through a tight helmet covering the head and neck. In the supine position heart rate increased about 10%, mean arterial pressure was unchanged, subcutaneous blood flow was unchanged, but skeletal muscle blood flow increased about 70%. Measurements were repeated during neck suction, -20 mmHg, and 45 degrees head-up tilt (which is known to decrease subcutaneous blood flow and skeletal muscle blood flow by increasing sympathetic vasoconstrictor activity). Heart rate increased by about 20%, mean arterial pressure was unchanged, subcutaneous blood flow was unchanged and skeletal muscle blood flow increased about 100%. These results indicate that skeletal muscle blood flow is modulated through carotid baroreceptors. Subcutaneous blood flow seems not to be influenced by high pressure baroreceptor modulation, although a vasoconstrictor response to head-up tilt was demonstrated in this as well as other recent studies.

Cardiovascular and respiratory effects of carotid body stimulation in the monkey.

1. The carotid bodies were stimulated in the anaesthetized pig-tailed macaque monkey (M. nemestrina) using (i) brief injections of cyanide or CO2-equilibrated bicarbonate solution into a common carotid artery, and (ii) longer perfusion with hypoxic hypercapnic blood in vascularly isolated chemoreceptor preparations. 2. In spontaneously breathing animals brief stimuli (thirty-one tests, seven monkeys) consistently increased pulmonary ventilation (by 97 +/- 10% of control), slowed the heart rate (the pulse interval increasing by 36 +/- 7.5%), and increased femoral vascular resistance (by 44 +/- 7%). 3. More sustained chemoreceptor stimulation with asphyxial blood (nineteen tests, five monkeys) increased ventilation by 187 +/- 23%, but transient bradycardia occurred in only eight of nineteen tests and was followed by tachycardia; in the remaining tests, only tachycardia occurred. After 20--40s, the pulse interval was 5.8 +/- 0.9% below the control level. Femoral vascular resistance either increased (five tests, two animals) or decreased (six tests, two animals). 4. Evidence is presented that in the monkey the autonomic effects of chemoreceptor stimulation are influenced by the level of respiratory activity with bradycardia and vasoconstriction occurring when the level is low, and tachycardia and vasodilatation when it is high. 5. The interaction of autonomic responses resulting from carotid body stimulation and from mechanisms initiated by the concomitant hyperventilation are qualitatively similar in the monkey and in subprimate species, although there may be quantitative differences such as would account for the species differences to distrubances produced, for instance, by arterial hypoxia.

Increased release of [ 3H]dopamine during low O 2 stimulation of rabbit carotid body in vitro

Rabbit carotid bodies synthesized [ 3H]dopamine (DA) during a 3-h incubation period in modified Tyrode's solution containing 40 μM [ 3H]tyrosine. Following this loading period, the carotid bodies were exposed for one additional hour to unlabelled Tyrode's solution equilibrated with either 10% oxygen in nitrogen or with 100% oxygen. The carotid bodies exposed to low O 2 released 81% more [ 3H]dopamine during this one-hour period than the carotid bodies exposed only to pure oxygen. These data suggest that hypoxia induces release of DA from the carotid body.

Cardiac norepinephrine output during carotid body stimulation.

In a series of 7 dogs, selective stimulation of the carotid body receptors by hypoxic blood produces an increase of coronary flow and greater release of norepinephrine from the heart; the increase of coronary flow is less marked and the release of norepinephrine is increased after vagotomy. Myocardial norepinephrine content is decreased by carotid body stimulation.

Coronary vascular and myocardial responses to carotid body stimulation in the dog.

Coronary vascular and myocardial responses to selective hypoxic and/or hypercapnic carotid chemoreceptor stimulation were investigated in constantly ventilated, pentobarbital or urethan-chloralose anesthetized dogs. Bilaterally isolated carotid chemoreceptors were perfused with autologous blood of varying O2 and CO2 tensions via an extracorporeal lung circuit. Systemic gas tensions were unchanged. Effects of carotid chemoreceptor stimulation on coronary vascular resistance, left ventricular dP/dt, and strain-gauge arch output were studied at natural coronary blood flow with the chest closed and during constant-flow perfusion of the left common coronary artery with the chest open. Carotid chemoreceptor stimulation slightly increased left ventricular dP/dt and slightly decreased the strain-gauge arch output, while markedly increasing systemic pressure. Coronary blood flow increased; however, coronary vascular resistance wa.as not affected. These studies show that local carotid body stimulation increases coronary blood flow but has little effect on the myocardium. The increase in coronary blood flow results mainly from an increase in systemic arterial pressure. Thus these data provide little evidence for increased sympathetic activity of the heart during local stimulation of the carotid chemoreceptors with hypoxic and hypercapnic blood.

Reflex vascular responses in kidney, ileum, and forelimb to carotid body stimulation.

Reflex vascular responses to local carotid chemoreceptor stimulation with hypoxic-hypercapnic, hypoxic, or hypercapnic blood were investigated in pentobarbitalized dogs. Bilaterally isolated carotid chemoreceptors were perfused via an extracorporeal lung circuit. Oxygen and carbon dioxide tensions of blood perfusing the carotid bodies were altered by ventilating the isolated lung with various O2-CO2 mixtures. Ventilation of the whole animal maintained normal systemic O2 and CO2 tensions. Perfusion pressures of the isolated kidney, ileum, forelimb, gracilis and hindpaw were measured during constant-flow perfusion. Carotid chemoreceptor stimulation with hypoxic-hypercapnic blood before vagotomy increased renal vascular resistance but caused no change in intestinal or forelimb resistance. Following vagotomy, hypoxic-hypercapnic, hypoxic, or hypercapnic carotid body stimulation increased renal, intestinal, and forelimb vascular resistance. Forelimb skin and muscle vascular beds contributed about equally to the increase in forelimb resistance. Gracilis muscle and hindpaw resistance also increased during hypoxic-hypercapnic stimulation after vagotomy.

Cardio-respiratory responses to carotid body stimulation with NaCN in the chicken

When a dose of NaCN of 0.10 mg/kg was injected intravenously into anesthetized chickens, there was an increase in respiratory minute volume. This increase was achieved primarily, but not entirely, by an increase in frequency. Heart frequency was elevated and blood pressure was depressed. These responses of the oxygen transport system are the ones usually reported for arterial hypoxia in the chicken. Injections of 0.01 mg/kg of NaCN into the carotid artery near the origin of the parathyroid artery caused a marked increase in the frequency and depth of respiration. In the chicken, there is a close association between the parathyroid gland and the carotid body. Thus it is likely that the respiratory response to the close-arterial injection was mediated by the carotid body chemoreceptor. The close-arterial injections of NaCN failed to produce statistically significant changes in heart frequency and blood pressure. Therefore, while these data demonstrate that the carotid body of the chicken plays a prominent role in the control of respiration, the role of the carotid body in cardiovascular control is not clear.

On the direct and crossed components of reflex responses to unilateral stimulation of the carotid body chemoreceptors in the dog.

1. In dogs under chloralose-urethane anaesthesia the chemoreceptors of the two carotid bodies were separately stimulated.2. The distribution of three primary reflex responses to carotid body stimulation was studied: parasympathetic bradycardia, sympathetic vasoconstriction, and increase in somatic phrenic nerve activity.3. The reflex bradycardia evoked by either carotid body was mediated by both vagus nerves, but when either vagus was blocked a greater response could be obtained from the contralateral than from the ipsilateral carotid body.4. The reflex vasoconstriction evoked by either carotid body was seen in both hind limbs, with no predominance in either limb.5. The reflex increase in phrenic nerve activity evoked by either carotid body was seen in both phrenic nerves, with no predominance in either nerve.

Carotid body: structure and function.

Through an unfortunate error in make-up of the article “Carotid Body: Structure and Function,” by T. J. Biscoe, in the July issue of this journal, two sections of the review are out of order. To co...

Integrative neural cardiovascular control.

Integrative neural cardiovascular control.

Regional circulatory responses to arterial hypoxia in the anesthetized dog.

ARTICLESRegional circulatory responses to arterial hypoxia in the anesthetized dogJA KrasneyJA KrasneyPublished Online:01 Mar 1971https://doi.org/10.1152/ajplegacy.1971.220.3.699MoreSectionsPDF (1 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByProne Position Impairs Oxygen Supply-Demand Balance During Systemic Hypoxia in RabbitsYonago Acta Medica, Vol. 64, No. 2 -Adrenergic regulation of systemic peripheral resistance and blood flow distribution in the turtle Trachemys scripta during anoxic submergence at 5 C and 21 CJournal of Experimental Biology, Vol. 207, No. 2Effects of α - and β -adrenergic stimulation on hepatosplanchnic perfusion and oxygen extraction in endotoxic shockCritical Care Medicine, Vol. 29, No. 3Acute cardiovascular response to isocapnic hypoxia. II. Model validationMauro Ursino, and Elisa Magosso1 July 2000 | American Journal of Physiology-Heart and Circulatory Physiology, Vol. 279, No. 1Effect of Independent Changes in Mixed-Venous PCO2or PO2on Cardiac Output in Anesthetized SheepJournal of Surgical Research, Vol. 71, No. 2Systemic pressor response during hindlimb ischemia is inversely related to femoral artery pressure and fractional inspired oxygenSurgery, Vol. 120, No. 5The oxygen consumption/oxygen delivery curve in severe preeclampsia: Evidence for a fixed oxygen extraction stateAmerican Journal of Obstetrics and Gynecology, Vol. 169, No. 6Coronary Hemodynamics and Myocardial Metabolism in Sepsis and Septic ShockEffect of acute and chronic moderate hypoxia on the kinetics of lidocaine and its metabolites and on regional blood flowPulmonary Pharmacology, Vol. 5, No. 1The coronary circulation and the myocardial oxygen supply/uptake relationship: A short reviewJournal of Critical Care, Vol. 6, No. 1Multiple Organ Oxygen Supply-Demand Relationships and Redistribution of FlowDistribution of systemic blood flow during anoxia in the turtle, Chrysemys scriptaRespiration Physiology, Vol. 78, No. 3Oxygen Delivery and Uptake by Peripheral Tissues: Physiology and PathophysiologyCritical Care Clinics, Vol. 5, No. 2Relation transport-consommation d'oxygène. Rôle d'une altération de l'extraction tissulaireAnnales Françaises d'Anesthésie et de Réanimation, Vol. 8, No. 6The concept of a critical oxygen deliveryIntensive Care Medicine, Vol. 13, No. 4Reflex Responses to Chemoreceptor Stimulation1 January 2011The Role of the Vasculature in the Regulation of Cardiac OutputCardiology Clinics, Vol. 4, No. 2Arterial Chemoreceptors1 January 2011The Role of the Vasculature in the Regulation of Cardiac OutputClinics in Chest Medicine, Vol. 4, No. 2The effect of digoxin on cardiovascular responses to hypoxia and reoxygenation in anesthetized dogsEuropean Journal of Pharmacology, Vol. 80, No. 2-3Effects of hypoxia on the closing pressure of the canine systemic arterial circulation.Circulation Research, Vol. 49, No. 4Direct effects of carbon monoxide on cardiac functionInternational Archives of Occupational and Environmental Health, Vol. 49, No. 1Effect of Local Metabolic Factors on Vascular Smooth Muscle1 January 2011Neural Control of the Circulation during HypoxiaSystemic hypoxia and hyperoxia, and liver blood flow and oxygen consumption in the greyhoundPfl�gers Archiv European Journal of Physiology, Vol. 381, No. 2Cardio-respiratory responses to carotid body stimulation with NaCN in the chickenRespiration Physiology, Vol. 17, No. 2 More from this issue > Volume 220Issue 3March 1971Pages 699-704 Copyright & PermissionsCopyright © 1971 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1971.220.3.699PubMed5545679History Published online 1 March 1971 Published in print 1 March 1971 Metrics

Effect of sino-aortic denervation on regional circulatory responses to cyanide.

ARTICLESEffect of sino-aortic denervation on regional circulatory responses to cyanideJA KrasneyJA KrasneyPublished Online:01 Jan 1970https://doi.org/10.1152/ajplegacy.1970.218.1.56MoreSectionsPDF (3 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByAutonomic control of the cardiovascular system in the cat during hypoxemiaAutonomic Neuroscience, Vol. 174, No. 1-2Cyanides1 January 2010Experimental, Clinical, Occupational Toxicology, and Forensic Aspects of Hydrogen Cyanide with Particular Reference to Vapor Exposure25 November 2009Is the aortic depressor nerve involved in arterial chemoreflexes in rats?Journal of the Autonomic Nervous System, Vol. 78, No. 1Effect of Independent Changes in Mixed-Venous PCO2or PO2on Cardiac Output in Anesthetized SheepJournal of Surgical Research, Vol. 71, No. 2Reflex and direct effects of sodium cyanide in anesthetized rats25 September 2008 | Archives Internationales de Physiologie, de Biochimie et de Biophysique, Vol. 102, No. 6Cyanide-related changes in cerebral O2 delivery and metabolism in fluorocarbon-circulated ratsToxicology and Applied Pharmacology, Vol. 94, No. 1Circulation to Skeletal Muscle1 January 2011Arterial Chemoreceptors1 January 2011Neural Control of the Circulation during HypoxiaCardio-respiratory responses to carotid body stimulation with NaCN in the chickenRespiration Physiology, Vol. 17, No. 2Blutdruckverhalten bei Anoxie nach intrabulbärer Unterbrechung des aortalen Chemoreflexbogens beim KaninchenArchiv für Kreislaufforschung, Vol. 64, No. 1-2 More from this issue > Volume 218Issue 1January 1970Pages 56-63 Copyright & PermissionsCopyright © 1970 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1970.218.1.56PubMed5409893History Published online 1 January 1970 Published in print 1 January 1970 Metrics

Chemical, electron microscopic and physiological observations on the role of catecholamines in the carotid body

Chemical determinations revealed large amounts of dopamine, noradrenaline and adrenaline, in the carotid body of the cat. The cathecholamine (CA) content of normally innervated and chronically synmpathectomized carotid bodies was essentially the same. It did not change by vigorous and prolonged carotid body stimulation either in situ or in vitro. High doses of reserpine reduced appreciably the noradrenaline content of the carotid body; the contents of dopamine and adrenaline also were reduced but to a lesser degree. Electron microscopy shoed the presence of numerous dense-cored vesicles in the glomus cells of the carotid body; these vesicles occurred only rarely in the capsular cells and in the carotid nerve terminals. No detectable change in the vesicular content, appearance or distribution was induced by prolonge dhypoxia, reserpinization, adrenalectomy or chronic section of the carotid nerve or sympathetic supply. Acute and chronic reserpinization of cats did not change the sensitivity and reactivity of carotid bodies (either in situ or in vitro to ACh, anoxic or asphyxic stimulation. In vitro, high doses of adrenaline, noradrenaline, dopamine, dl-DOPA and tyramine failed to produced chemoreceptor excitation or marked depression of the chemosensory discharges. The lack of effect of CA on chemoreceptor activity was not changed by reserpinization or inactivation of monaminoxidase with nialamide. Prolonged superfusion with dischloroisoproterenol, a β-adrenergic blocking agent, reduced chemoreceptor discharges by inducing nerve block. It is concluded that CA contained in the carotid body do not play a significant role in the generation of the chemosensory discharges.