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PubMed1981

Cerebrovascular response to hypoxia in baroreceptor- and chemoreceptor-denervated dogs.

Cerebral hemodynamic responses to arterial hypoxemia were studied in anesthetized paralyzed dogs that were or that had undergone carotid baroreceptor denervation, carotid chemoreceptor denervation, vagotomy, or both vagotomy and carotid sinus nerve section. Arterial O2 content was lowered from control (19.0 vol%) to 9.6 vol% by either decreasing arterial O2 tension [hypoxic hypoxemia (HH)] or increasing carboxyhemoglobin saturation[carbon-monoxide hypoxemia (COH)] at normal O2 tension. In intact animals (composite control values from all groups) HH and COH resulted in similar increases in cerebral blood flow (to 205 and 197% of control, respectively). Cerebral vascular resistance decreased more with COH than with HH (to 42 vs. 60% of control). The response from carotid baroreceptor-denervated animals and from vagotomized animals did not differ from that of the intact animals. After carotid chemoreceptor denervation and combined carotid sinus nerve section and vagotomy, both HH and COH increased cerebral blood flow to 194% of control (same increase as in intact animals, carotid baroreceptor-denervated animals, and vagotomized animals) and produced equal reductions in cerebral vascular resistance (to 34% of control). These data show that the carotid and aortic chemoreceptors are not necessary for the increase in cerebral blood flow provoked by hypoxemia and that this response is not modified by the carotid and aortic baroreceptors.

Animals↗

PubMed1982

Denervation of arterial chemoreceptors and baroreceptors in fetal lambs in utero.

Arterial baroreceptors and chemoreceptors were denervated in eight fetal lambs in utero. Carotid sinus and carotid body denervation was accomplished by stripping the carotid artery rostral and caudal to the origin of the occipital and lingual arteries. Aortic bodies were denervated by section of the superior laryngeal nerve and aortic nerve in the neck. The anatomy relevant to the technique is presented. The effectiveness of the denervation was tested by injection of 20 micrograms phenylephrine. The slowing of the fetal heart rate normally present in the intact lambs was abolished in the denervated fetuses. Denervation of the carotid and aortic chemoreceptors abolished the reflex bradycardia following injection of 200 micrograms cyanide or following acute hypoxemia produced by uterine blood flow reduction for 20 s. These results indicate that the baroreflex and chemoreflex can be elicited in utero and eliminated by the method we described. The preparation we present allows the study of the role of the arterial chemoreceptors and baroreceptors in normal fetal cardiovascular regulation and in fetal responses to stress.

Animals↗

PubMed1988

Peripheral chemoreceptor control of neurohypophysial blood flow.

Neurohypophysial blood flow responses to hypoxic hypoxia were studied under conditions of vagotomy, carotid sinus denervation, and combined vagotomy and carotid sinus denervation. Arterial O2 tension was lowered from 128 +/- 3 to 31 +/- 1 Torr, whereas pH and arterial CO2 tension remained constant. Denervation of either carotid sinus or aortic arch chemoreceptors alone does not attenuate the dilation of neurohypophysial vessels that accompanies hypoxic hypoxia. Combined denervation, however, completely blocks this response for the neurohypophysis but not for any other brain region studied. Hypoxic hypoxia resulted in an increase in plasma vasopressin (AVP) from approximately 8 to approximately 40 pg/ml. This increase occurred in the intact, vagotomy, and carotid sinus-denervation conditions. This neurosecretory response was also completely inhibited by combined denervation. For most brain regions peripheral chemoreceptors are not involved in the blood flow response; however, the response of the neurohypophysis appears to be mediated via these chemoreceptors, presumably by altering the neuroeffector activity to this region. In addition our data suggest a temporal relationship between neurohypophysial vasodilation and neurosecretion of AVP.

Animals↗

PubMed2003

Peripheral O2 chemoreceptors mediate humoral catecholamine secretion from fish chromaffin cells.

This study addressed the hypothesis that the secretion of catecholamines from trout (Oncorhynchus mykiss) chromaffin cells, during hypoxia, is triggered by stimulation of O(2) chemoreceptors located within the gills. Sodium cyanide was administered into the inspired water (external cyanide) or injected into the gill circulation (internal cyanide) to pharmacologically stimulate external (water sensing) or internal (blood sensing) O(2) chemoreceptors, respectively. Both of these treatments caused an elevation of circulating catecholamine levels. The response to external, but not internal, cyanide was abolished by removal of the first gill arch. Hypoxia produced an increase in circulating catecholamine levels that was unaffected by removal of the first gill arch or by denervation of the pseudobranch. Cyanide and hypoxia both caused the well-documented cardiorespiratory reflexes normally observed in this species. This study demonstrates, for the first time, that gill O(2) chemoreceptors can initiate the reflex that leads to catecholamine release from the chromaffin cells and that stimulation of internally oriented O(2) receptors on all gill arches appears to be the physiologically important mechanism for initiating release.

Animals↗

PubMed1984

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.

Amygdala↗

PubMed1989

Peripheral arterial chemoreceptors and reflex control of sodium and water homeostasis.

In response to acute exposure to moderate high-altitude hypoxia, mammals increase their blood hemoglobin concentration very rapidly by reducing their plasma volume. This phenomenon is caused not only by a redistribution of the body fluid volumes but also by a suppression of voluntary sodium and water intake as well as an inhibition of renal tubular sodium reabsorption with natriuresis and diuresis. This article reviews the role of the peripheral arterial chemoreceptors within the framework of the reflex mechanisms that might cause the changes in sodium and water metabolism in acute arterial hypoxia. The evidence that the peripheral arterial chemoreceptors do also influence sodium and water homeostasis in normoxia is presented. The interrelations between carotid body structure and arterial chemoreceptor reflex effects on the one hand and primary systemic hypertension on the other are discussed.

Animals↗

PubMed1990

Propranolol inhibits O2-sensitive chemoreceptor activity in trout gills.

The effects of propranolol on the activity of O2-sensitive chemoreceptors innervated by cranial nerve IX were studied using an isolated, perfused first gill arch preparation from rainbow trout (Onchyrhyncos mykiss). Perfusing the gill with hypoxic perfusate resulted in an increase in chemoreceptor activity. Propranolol (100-200 nmol) added to the perfusate inhibited O2-receptor discharge during both normoxia and hypoxia and attenuated the response to bolus injections of NaCN (25 micrograms). These results suggest that a beta-adrenergic mechanism is involved in O2 chemoreception. They further suggest that the inhibitory effects of propranolol on branchial, O2-sensitive chemoreceptors may contribute to the attenuated hypoxic ventilatory reflex observed in intact fish after propranolol injections.

Animals↗

PubMed1990

Reduced renal perfusion pressure causes prostaglandin-dependent excitation of R2 chemoreceptors in rats.

The activity of multiunit preparations of afferent renal nerve activity (ARNA) and single R2 chemoreceptors was recorded during graded reductions in renal perfusion pressure (RPP) produced by tightening an aortic snare in anesthetized rats. In 13 multiunit preparations an initial RPP reduction from 117 +/- 2 to 101 +/- 2 mmHg caused ARNA to increase 29 +/- 5% above control. Further reductions in RPP produced a 65 +/- 11% increase in ARNA at 80 +/- 1 mmHg, 87 +/- 24% at 59 +/- 1 mmHg, and 127 +/- 38% at 37 +/- 1 mmHg (P less than 0.01 ARNA vs. RPP). Renal blood flow was measured by pulsed Doppler flowmeter in these rats and showed good autoregulation and minimal reduction (-4 +/- 2%) during the initial pressure drop. Ten single R2 chemoreceptors increased their firing rate by 129 +/- 4% when RPP was reduced from 109 +/- 2 to 85 +/- 2 mmHg and showed a peak response of 494 +/- 105% at 27 +/- 2 mmHg. The activity of 11 R2 receptors increased from 3.7 +/- 1.0 to 6.8 +/- 0.8 impulses/10 s when RPP was reduced from 112 +/- 4 to 79 +/- 2 mmHg. Prostaglandin blockade with indomethacin (6 rats) or meclofenamate (7 rats) caused a decrease in basal activity in the same units to 1.8 +/- 0.5 impulses/10 s and eliminated their excitatory response to a similar reduction in RPP (108 +/- 4 to 75 +/- 3 mmHg). These data support a role for R2 chemoreceptors in neurocirculatory reflexes elicited by reductions in RPP.

Afferent Pathways↗

PubMed1994

Role of central chemoreceptors in behavioral thermoregulation of the toad, Bufo marinus.

We tested the hypothesis that hypercapnia will induce behavioral hypothermia in toads and that central chemoreceptors are involved in this response. Animals were tested in an enclosed temperature gradient supplied with different gas mixtures. Fractional inspired CO2 (FICO2) between 0 and 0.05 had no significant effect on selected body temperature, but FICO2 between 0.06 and 0.10 reduced the selected body temperature from U approximately 28 to 18 degrees C. To determine if the hypercapnia-induced hypothermia is mediated by acidification of central chemoreceptors, the pH of the fourth ventricle was kept constant by perfusion with mock cerebrospinal fluid of pH 7.7 or 7.1 (normal and acidic values, respectively). Ventricular perfusion at pH 7.7 under normocapnic conditions had no effect on body temperature. Hypercapnia (FICO2 0.08) failed to induce hypothermia when the fourth ventricle was kept at pH 7.7 and when hyperoxia was present. Acidic ventricular perfusion under normocapnic conditions decreased selected body temperature from 27 to 25 degrees C, a significant drop but much less than that due to hypercapnia producing the same brain pH, suggesting an important role of peripheral chemoreceptors. The physiological significance of behavioral hypothermia and nature of the peripheral stimulus were evaluated by measuring the effect of hypercapnia on arterial oxygen saturation, PO2, and pH at 15 and 25 degrees C. Arterial oxygen saturation was higher at the lower temperature. Increasing FICO2 decreased oxygen saturation at 25 degrees C but not at 15 degrees C. Arterial PO2 increased with increasing inspired CO2. This increase was greater at 15 degrees C than at 25 degrees C. Arterial pH decreased at both temperatures.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1996

NTS neurons with carotid chemoreceptor inputs arborize in the rostral ventrolateral medulla.

Neurons that were excited by hypoxic stimulation of carotid chemoreceptors were recorded in the caudal portion of the nucleus of the solitary tract (cNTS) of urethan-anesthetized, vagotomized, aortic-deafferented, artificially ventilated rats (n = 23). The focus of the study is on 26 chemosensitive neurons (classified as early- and late-response cells) that were tonically activated by chemoreceptor stimulation and never fired in bursts synchronized with the phrenic nerve discharge (PND) cycle. The discharge of early-response cells (n = 14) started up to 2.5 s before the onset of PND activation, whereas the discharge of late-response cells (n = 14) started 1.5-5 s after onset of PND response. Four early-response cells were antidromically activated from the rostral ventrolateral medulla (RVLM; latencies: 7-13 ms), and two had axenal collaterals in the region of the nucleus ambiguus. Four late-response neurons were antidromically activated from the RVLM (latencies: 6-12 ms), but no collateral was found in this area. The basal discharge of early- and late-response cells ranged from 0 to 10 and 0 to 30 spikes/s, respectively, but most of them had a very low spontaneous firing rate (median: 0.2 and 0.6 spikes/s, respectively). Neither type was excited by baroreceptor stimulation. The cNTS also contained neurons that were firing in bursts synchronized with the PND cycle. These cells were activated by chemoreceptor stimulation and were not antidromically activated from the RVLM. Chemosensitive neurons made up 33% of cNTS neurons antidromically activated from the RVLM (8/24). In conclusion, a population of cNTS chemosensitive neurons devoid of respiratory modulation projects through the RVLM and arborizes in this region.

Afferent Pathways↗

PubMed1997

Trigeminal and chemoreceptor contributions to bradycardia during voluntary dives in rats.

This study investigates the importance of chemoreceptive and trigeminal information during voluntarily initiated diving in rats. The heart rate responses to simulated diving are unaffected by chemoreceptor drive [McCulloch, P.F., and N. H. West. Am. J. Physiol. 263 (Regulatory Integrative Comp. Physiol. 32): R1049-R1056, 1992] but are reversibly eliminated by infusion of glutamate receptor antagonists into the spinal trigeminal nuclei [McCulloch, P. F., I. A. Paterson, and N. H. West. Am. J. Physiol. 269 (Regulatory Integrative Comp. Physiol. 38): R669-R677, 1995]. To investigate the role of chemoreceptor drive in conscious dives, rats were made hypercapnic, hyperoxic, or hypoxic predive. The role of trigeminal input was explored by infusing the glutamatergic antagonists D-2-amino-7-phosphoheptanoic acid and 6,7-dinitroquinoxaline-2,3-dione into the region of the trigeminal nuclei. The alteration of arterial blood gases predive had no effect on diving bradycardia. Trigeminal blockade reduced the intensity of the bradycardia but did not abolish it. Chemoreceptor input does not play a significant role in determining heart rate during conscious diving in rats. The attenuation, rather than abolition, of bradycardia on trigeminal blockade suggests either that we achieved incomplete blockade or that an additional spectrum of sensory inputs not present in simulated diving is important in determining the underwater heart rate during conscious diving in rats.

Animals↗

PubMed2001

Differential chemoreceptor reflex responses of adrenal preganglionic neurons.

Adrenal sympathetic preganglionic neurons (ADR SPNs) regulating the chromaffin cell release of epinephrine (Epi ADR SPNs) and those controlling norepinephrine (NE ADR SPNs) secretion have been distinguished on the basis of their responses to stimulation in the rostral ventrolateral medulla, to glucopenia produced by 2-deoxyglucose, and to activation of the baroreceptor reflex. In this study, we examined the effects of arterial chemoreceptor reflex activation, produced by inhalation of 100% N(2) or intravenous injection of sodium cyanide, on these two groups of ADR SPNs, identified antidromically in urethane-anesthetized, artificially ventilated rats. The mean spontaneous discharge rates of 38 NE ADR SPNs and 51 Epi ADR SPNs were 4.4 +/- 0.4 and 5.6 +/- 0.4 spikes/s at mean arterial pressures of 98 +/- 3 and 97 +/- 3 mmHg, respectively. Ventilation with 100% N(2) for 10 s markedly excited all NE ADR SPNs (+222 +/- 23% control, n = 36). In contrast, the majority (40/48; 83%) of Epi ADR SPNs were unaffected or slightly inhibited by ventilation with 100% N(2) (population response: +6 +/- 10% control, n = 48). Similar results were obtained after injection of sodium cyanide. These observations suggest that the network controlling the spontaneous discharge of NE ADR SPNs is more sensitive to brief arterial chemoreceptor reflex activation than is that regulating the activity of Epi ADR SPNs. The differential responsiveness to activation of the arterial chemoreceptor reflex of the populations of ADR SPNs regulating epinephrine and norepinephrine secretion suggests that their primary excitatory inputs arise from separate populations of sympathetic premotor neurons and that a fall in arterial oxygen tension is not a major stimulus for reflex-mediated adrenal epinephrine secretion.

Adrenal Glands↗

PubMed1975

Nonperipheral chemoreceptor stimulation of ventilation by cyanide.

To assess the ventilatory responses elicited by changes of tissue hypoxia, sodium cyanide (0.12 mg/kg-min for 10 min) was infused into the upper abdominal aorta of anesthetized dogs. These infusions produced decreases in oxygen consumption, increases in arterial lactate concentration, and increases in arterial lactate/pyruvate ratio. Coincident with these metabolic changes of hypoxia, minute ventilation (VE) increased 228 +/- SE 36% and arterial PCO2 decreased 21 +/- SE 2 mmHg; therefore, pH increased both in arterial blood in and cisternal cerebrospinal fluid. Following infusion of cyanide into the abdominal aorta, small quantities of cyanide (48 +/- SE 14 mumol/liter) appeared in carotid arterial blood. To evaluate the possibility that the observed increases in VE were due to stimulation of peripheral arterial chemoreceptors by the recirculating cyanide, the carotid and aortic chemoreceptors were denervated in four dogs. Nonetheless, after intra-aortic infusion of sodium cyanide (1.2 mg/kg), ventilation in these chemodenervated animals again increased considerably (154 +/- SE 36%). In order to explore the possibility that cyanide infusion can stimulate ventilation by an extracranial mechanism, heads of vagotomized dogs (including the carotid bodies) were perfused entirely by donor dogs. The intra-aortic infusion of sodium cyanide (0.9 mg/kg) into these head-perfused animals still caused large increases in VE (163 +/- SE 19%). It is concluded that intra-aortic cyanide infusions stimulate VE by an extracranial mechanism other than the carotid and aortic chemoreceptors.

Animals↗

PubMed1975

Ventilatory interaction between hypoxia and [H+] at chemoreceptors of man.

By measuring ventilation during isocapnic progressive hypoxia, peripheral chemoreceptor sensitivity to acute hypoxia (deltaV40) was measured in five normal young men under four sets of conditions: 1) at sea level at the subject's resting PCO2, 2) at sea level with PCO2 5 Torr above resting PCO2, 3) after 24 h at a simulated altitude of 4,267 m (PB = 447 Torr) at the subject's resting PCO2 measured during acute hyperoxia, and 4) after 24 h at high altitude, with PCO2 elevated to the subject's sea-level resting PCO2. With this experimental design, we were able to systematically vary the PCO2 and [H+] at the peripheral and central chemoreceptors of man. When mean pHa was decreased from 7.424 to 7.377 without significant change in PACO2, the mean deltaV40 increased from 18.0 to 55.9 1/min. Conversely, when mean PACO2 was altered between 33.8 and 41.6 Torr with pHa held relatively constant, the mean deltaV40 did not change. This suggests that it is the H+ and not CO2 which interacts with hypoxia in stimulating the ventilation of man. An additional finding was that the intrinsic sensitivity of the peripheral chemoreceptors to acute hypoxia did not change during 24 h of acclimatization to high altitude.

Adult↗

PubMed1976

Ventilatory control in peripheral chemoreceptor-denervated ponies during chronic hypoxemia.

The present study was designed to provide further insight into the role of the carotid and aortic chemoreceptors in ventilatory (VE) acclimatization during sojourn at altitude. Measurements were made: 1) on 10 ponies near sea level (SL, 740 Torr) under normal conditions, 2) on 6 of these at SL following chemoreceptor denervation (CD), and 3) subsequently on all 10 during 4 days of hypobaric hypoxia (PaO2 = 40-47 Torr). CD resulteo in hypoventilation at SL (deltaPaCO2 = d8 Torr, P less than 0.05), and it prevented hyperventilation normally observed with injection of NaCN and acute exposure to hypoxia (less than 1 h). In contrast, hyperventilation was evident in normal ponies during acute hypoxia (deltaPaCO2 = -6.7 Torr). Ventilation increased in both groups between the 2nd and 8th h of hypoxia (deltaPaCO2 from 1 h = -4 Torr, P less than 0.05). This change, a common characteristic of acclimatization, persisted throughout 4 days of hypoxia in the normal ponies. However, in the CD ponies this change was evident consistently only through the 12th h and after the 44 h hyperventilation was no longer evident. We conclude that the peripheral chemoreceptors are essential in ponies for normal VE acclimatization to this degree of hypoxemia. Two additional findings in CD ponies suggest the presence of a CNS inhibitory influence on the VE control center during chronic hypoxemia. First, acute hyperoxygenation on the 4th day of hypoxemia induced hyperventilation (deltaPaCO2 = -5 Torr, P less than 0.05). Second, again on the 4th day and during hyperoxygenation, VE responsiveness to CO2 and doxapram HCl was greater than at sea level.

Acclimatization↗

PubMed1977

Carotid and aortic chemoreceptor function in the rat.

Carotid and aortic chemoreceptor function was studied in normal Wistar rats. Sodium cyanide, lobeline HCl, and doxapram HCl in the doses of 2-400 mug/kg injected into the external carotid artery stimulated respiration significantly. Injections of the drugs into the ascending aorta produced less effects which were abolished after section of the carotid sinus nerves. The drugs produced a significant increase in the carotid sinus nerve activity but failed to do so in the aortic depressor or recurrent laryngeal nerves. These results indicate that the carotid chemoreceptor function in Wistar rats in normal while functional aortic chemoreceptors are absent in them.

Action Potentials↗

PubMed1981

On chemoreceptor control of ventilatory responses to CO2 in unanesthetized ducks.

Using cross perfusion between pairs of animals we examined the effects of increases in arterial CO2 tension (Paco2) at pulmonary, carotid body, and central chemoreceptors on ventilation in unanesthetized, spontaneously breathing White Pekin ducks. By adjusting the level of inspired CO2 of either the experimental or donor animals it was possible to manipulate Paco2 at any one or combination of the receptor groups. Stimulation of central chemosensitive areas alone was three to four times more effective in increasing both frequency and minute ventilation (Ve) than stimulation of the carotid bodies alone. Increases in tidal volume were small in both instances. Increasing PCO2 in the pulmonary circulation of an innervated lung, independent of changes in Paco2 at the carotid body or head, had no effect on VE. We conclude that central chemoreceptors play the major role in a steady-state response of awake ducks to CO2 while the carotid bodies play a smaller but still significant role. The intrapulmonary chemoreceptors play no role in the response per se although their inhibition by high airway CO2 causes marked effects on the pattern of breathing

Animals↗

PubMed1981

Respiratory neuron responses to hypercapnia and carotid chemoreceptor stimulation.

In decerebrate, vagotomized, paralyzed, and ventilated cats, activities were recorded from the phrenic nerve and from respiratory units within the dorsal and ventral medullary respiratory nuclei and the pontile reticular formation. These unit activities were monitored during equivalent augmentations in peak integrated phrenic nerve activity induced by stimuli acting primarily on the peripheral or central chemoreceptors. These stimuli were intracarotid infusions of sodium cyanide or nicotine and exposure to hyperoxic hypercapnia, respectively. Both stimuli caused similar increases in activities for most dorsal nucleus inspiratory units. For units of the ventral medullary nucleus, augmentations in activity were only significant (inspiratory neurons) or were of greater magnitude (expiratory neurons) during hypercapnia. As opposed to medullary units, the discharge frequencies of many pontile units were unaltered or declined during both peripheral and central chemoreceptor stimulations. These results support the concept that excitatory influences from the peripheral and central chemoreceptors are not equally distributed among all groups of brain stem respiratory neurons.

Animals↗