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The responses of chemoreceptors at reduced temperatures.

1. The responses of aortic chemoreceptors and pulmonary stretch receptors of cats were studied by recording impulses in individual fibres at normal body temperatures and thereafter at various temperatures down to 24-26 degrees C while cooling the cat with ice.2. Reduction of metabolism by lowering the temperature did not obviously slow the P(O2) sensing mechanism of chemoreceptors but it greatly slowed the development of excitation after circulatory arrest. It also greatly reduced the excitatory effect of hypoxia.3. The Q(10) for the frequency of discharge of chemoreceptors (during maximal activity) was estimated by comparing the activity of the endings at normal body temperature after circulatory arrest (i.e. at a local P(O2) of 0 mm Hg) with similar activity at reduced body temperatures. This averaged 2.5 in nine endings. The Q(10) for the peak frequency of discharge also averaged 2.5 in seven endings. These values are similar to those of some mechano-receptors.4. Apart from the reduction in the frequency of discharge (Q(10) = 2.6) lowering the temperature did not alter the stimulus-response relationship of pulmonary stretch receptors.5. The poor responses to ACh at lower temperatures indicate that ACh is not likely to be a transmitter at chemoreceptors.

Acetylcholine↗

Respiratory modulation of barareceptor and chemoreceptor reflexes affecting heart rate and cardiac vagal efferent nerve activity.

1. Brief stimuli were delivered to the carotid chemoreceptors or baroreceptors in dogs anaesthetized with chloralose. Chemoreceptor stimulation was achieved by rapid retrograde injection of 0.2-0.5 ml. CO2 equilibrated saline through a cannula in the external carotid artery. Baroreceptor stimulation was achieved by forceful retrograde injection of 2-5 ml. air-equilibrated saline into the external carotid artery after first clamping the common carotid artery. 2. prompt decreases in heart rate were elicited by brief sudden chemoreceptor or baroreceptor stimuli when these were delivered during the expiratory phase of respiration. The stimuli did not modify the control heart rate pattern when delivered in the inspiratory phase of respiration. This respiratory modulation of reflex effectiveness persisted when the animals were completely paralysed and the phase of the respiratory cycle was monitored through a phrenic electroneurogram. 3. single cardiac vagal efferent nerve fibres were dissected from the cut central end of the right cervical vagus nerve. They were classified as cardiac efferents by their cardiac and respiratory rhythmicity, and by their increased activity in response to stimulation of a carotid sinus nerve or to mechanical elevation of the systemic arterial pressure. These efferent fibres increased their activity in response to brief chemoreceptor or baroreceptor stimuli delivered in expiration, but did not respond to stimuli delivered in inspiration. This respiratory modulation of both reflexes persisted after bilateral cervical vagotomy.

Animals↗

The location of carbonic anhydrase in relation to the blood-brain barrier at the medullary chemoreceptors of the cat.

1. The role of carbonic anhydrase near the medullary chemoreceptors has been investigated in the cat. Vertebral artery injections have been used to cause abrupt changes in respiration as a result of changes in the activity of medullary chemoreceptors. 2. Injections of 100% CO2-saline were used to stimulate respiration and of Tris or alkalinized albumin solution to cause a reduction in respiration. 3. The injections gave rapid effects. We studied the effect on these of benzolamide (1-4 mg/kg i.v.) a carbonic anhydrase inhibitor which does not easily cross the blood-brain barrier and acetazolamide (50 mg/kg i.v.) an inhibitor which crosses the barrier more easily. 4. The effects of Tris were much reduced after benzolamide. Even addition of benzolamide to the injected Tris or albumin was sufficient to reduce their effects. 5. The effects of CO2-saline were reduced only after acetazolamide i.v. Whereas addition of carbonic anhydrase to injected Tris potentiated the effects on respiration, after acetazolamide this potentiation was much less marked. 6. It is concluded that carbonic anhydrase acts in the region of the medullary chemoreceptors at two sites: (a) outside the blood-brain barrier, probably at the luminal surface of the capillary endothelium, where it may act on plasma buffers, and (b) inside the barrier, in association with the chemoreceptors, where it may accelerate CO2/pH equilibration.

Animals↗

The pattern of cardiovascular response to carotid chemoreceptor stimulation in the cat.

1. The pattern of cardiovascular response evoked by carotid chemoreceptor stimulation has been investigated in cats anesthetized by continuous infusion of Althesin (Glaxo). 2. A variety of chemoreceptor stimulants, injected retrogradely into the lingual artery with the external carotid artery ligated, evoked hyperventilation with variable changes in arterial pressure and heart-rate, but a consistent vasodilatation in limb muscles and vasoconstriction in renal, mesenteric and cutaneous vasculature. 3. The muscle vasodilatation was still obtained after vagotomy and when the animal was paralysed and artificially ventilated; thus, it was not secondary to the hyperventilation. 4. In the majority of experiments the muscle vasodilatation was much reduced or abolished by atropine indicating it was mediated by sympathetic cholinergic fibres, which is characteristic of the alerting stage of the defence reaction in the cat. The cardiovascular pattern was accompanied by the other autonomic features of the alerting response, viz. pupillary dilatation, retraction of the nictitating membranes and pilo-erection. 5. In one and the same animal the pattern of response evoked by carotid chemoreceptor stimulation was the same as that evoked by noxious cutaneous stimulation, and by electrical stimulation in the brain stem defence areas. 6. It is concluded that peripheral chemoreceptor stimulation acts as an excitatory input to the hypothalamic and brain stem defence areas and that it can readily evoke the autonomic components of the alerting stage of the defence reaction. It is suggested that this has been missed in previous studies on anaesthetized animals because of the depressant action of chloralose and barbiturates on transmission in the hypothalamus and mid-brain.

Animals↗

Effects of stimulation of aortic chemoreceptors on abdominal vascular resistance and capacitance in anaesthetized dogs.

1. Dogs were anaesthetized with chloralose, ventilated artificially, and the regions of the aortic arch and carotid sinuses were isolated vascularly and perfused with blood. The abdominal circulation was isolated vascularly, perfused at constant flow and drained from the inferior vena cava at constant venous pressure. Changes in vascular resistance were determined by calculating changes in abdominal aortic perfusion pressure, and changes in capacitance by integrating the changes in venous outflow. 2. Stimulation of aortic body chemoreceptors, either by changing the aortic arch perfusate from arterial to venous blood at constant perfusion pressure or by injection of sodium cyanide into the aortic arch, resulted in an increase in abdominal vascular resistance and a decrease in abdominal vascular capacitance. 3. After both cervical vagosympathetic trunks had been cut, stimulation of aortic chemoreceptors no longer resulted in resistance or capacitance responses. 4. These results indicate that stimulation of aortic chemoreceptors, like carotid chemoreceptors, results in reflex constriction of both resistance and capacitance vessels in the abdominal circulation.

Abdomen↗

Neural respiratory and circulatory interaction during chemoreceptor stimulation and cooling of ventral medulla in cats.

The effects on respiratory and sympathetic neural activity, measured as integrated phrenic and cervical nerve activities respectively, during changing input from the central chemoreceptors was studied in anaesthetized, paralysed cats whose carotid sinus nerves and vagus nerves had been cut. Central respiratory drive was altered either by graded cold block of the intermediate areas, located bilaterally near the ventral surface of the medulla oblongata, or by step increases in end-tidal PCO2. Cervical nerve activity showed both a tonic (or mean) level of activity and a prominent cyclic discharge that was in phase with phrenic nerve activity. Graded focal cooling of the intermediate areas to 20 degrees C when end-tidal PCO2 was kept constant caused progressive decreases in phrenic activity, the amplitude of the inspiratory related discharge and mean arterial pressure, but only a small decrease in mean cervical nerve activity. Cooling the intermediate areas in the absence of the inspiratory related discharge (i.e. when phrenic activity was below the apnoeic threshold) led to a much smaller decrease in arterial pressure. Step increases of end-tidal PCO2 caused progressive increases of both cervical and phrenic nerve activities. The increase in cervical activity was due primarily, if not wholly, to a progressive increase in the amplitude of the inspiratory related discharge. These findings show that the predominant effect on sympathetic activity during stimulation of the central chemoreceptor and graded cold block of the intermediate areas is a change in the amplitude of the inspiratory related discharge and suggest that the change in arterial pressure that accompanies central chemoreceptor stimulation and graded cold block of the intermediate areas is mediated by the inspiratory related discharge rather than by an increase in the mean level of sympathetic activity. When phrenic activity was lowered to below apnoeic threshold by cooling the intermediate areas, step increases in end-tidal PCO2 caused inhibition rather than stimulation of cervical nerve activity. This finding indicates that sympathetic neurones are not activated by central chemoreceptor input directly, but rather indirectly via intracranial connexions with neuronal networks involved in regulation of respiration.

Action Potentials↗

Modification by lung inflation of the vascular responses from the carotid body chemoreceptors and other receptors in dogs.

The reflex effects of increasing pulmonary ventilation on the responses of the hind-limb and systemic vascular resistances to stimulation of the carotid body chemoreceptors and carotid sinus baroreceptors and to distension of the urinary bladder have been studied in the anaesthetized dog. A preparation was used incorporating total cardiopulmonary bypass to maintain the arterial blood gas composition constant when alterations in pulmonary ventilation were made. The regions of both carotid bifurcations, the arch of the aorta and the cerebral circulation were independently perfused at constant pressure so as to exclude secondary reflexes from arterial baroreceptors. Four levels of pulmonary ventilation were used: 0.095, 0.285, 0.475 and 0.665 l min-1 kg-1 body weight, at a constant frequency of 19 cycles min-1. Increasing the pulmonary ventilation per se in steps from 0.095 to 0.665 l min-1 kg-1 resulted in a significant progressive reduction in hind-limb and systemic vascular resistances which were shown to be due to a reflex from the lungs. Stimulation of the carotid body chemoreceptors by hypoxic hypercapnic blood resulted in an increase in hind-limb and systemic vascular resistances when carried out at each of the four levels of pulmonary ventilation. The size of the increases in vascular resistances, however, was progressively and significantly reduced as the pulmonary ventilation was increased. This partial inhibition of the carotid body reflex vasoconstrictor response was dependent on the innervation of the lungs. Stimulation or unloading of the carotid sinus baroreceptors by altering the perfusion pressure in the vascularly isolated carotid bifurcation regions caused a significant decrease and increase respectively in hind-limb and systemic vascular resistances at all four levels of pulmonary ventilation. Unlike the responses to chemoreceptor stimulation, the size of these responses was unaffected by the level of pulmonary ventilation. Distension of the urinary bladder resulted in a significant increase in hind-limb and systemic vascular resistances. The size of these responses was also unaltered by changing the level of pulmonary ventilation. These results indicate that there is an interaction between the inputs from the lungs and the carotid body chemoreceptors in the control of hind-limb and systemic vascular resistances. In contrast the inputs from the carotid sinus baroreceptors and the urinary bladder were unaffected by the input from the lungs.

Animals↗

The effect of exercise on the central-chemoreceptor threshold in man.

1. The threshold of the central chemoreceptors was determined under resting and three exercise conditions in four volunteers. 2. The method used was the hyperoxic, Read rebreathing technique with prior hyperventilation. Plots of resting ventilation vs. carbon dioxide consisted of two straight-line segments of different slopes above and below a breakpoint which was taken as the central-chemoreceptor threshold at rest. 3. The threshold during exercise was determined from plots of exercise ventilation vs. carbon dioxide in a similar way, but the points for these plots were obtained in a different manner. They were obtained from a number of separate rebreathing experiments, so as to avoid the divergence between mouth and central-chemoreceptor carbon dioxide levels during rebreathing in exercise. 4. Exercise was started abruptly during rebreathing experiments similar to those at rest, at a particular level of carbon dioxide, and exercise ventilation was measured at the third breath. Each rebreathing experiment therefore provides one point for the exercise ventilation vs. carbon dioxide plot. 5. The results showed that the central-chemoreceptor threshold during exercise was not different from the resting threshold, and that the initial, fast component of exercise ventilation was independent of the chemical drive to breathe.

Adult↗

Do oxygen tension variations contribute to the respiratory oscillations of chemoreceptor discharge in the cat?

1. A high-frequency high-flow ventilator has been developed which will produce abrupt changes in alveolar gas tensions. We have used it to study the individual contributions of PCO2 and PO2 in producing the oscillations which occur in the discharge of carotid chemoreceptors in the cat with respiration, by producing repeated end-tidal alternations (i) of PCO2 in constant hypoxia, (ii) of PO2 in constant normocapnia and (iii) of both PO2 and PCO2, i.e. of asphyxia. 2. The chemoreceptor response to alternations of PCO2 was always brisker than that to alternations of PO2 at 2, 4 or 8 s cycle durations. 3. An increase in the frequency of the alveolar alternation shortened the difference between the response times to PCO2 and PO2 but it increased the phase difference between the stimulus and the response waveforms. 4. With 4 s cycles, in normocapnic hypoxia, PCO2 was 2.9 times more effective (impulses s-1 Torr-1) than PO2 in producing oscillations in discharge. 5. The oscillations in discharge to simultaneous alternations of PO2 and PCO2 were not significantly different from the sum of individual oscillations to alternations of PCO2 and of PO2 alone. This was true with respect to timing and to amplitude of the oscillation. 6. Usually the amplitude of the chemoreceptor discharge oscillation in response to an asphyxial alternation was greater than the amplitude of the oscillation to either its PCO2 or its PO2 component alone. However, at the highest frequencies used, the phase relation between the PCO2 and PO2 components of the response could lead to the summed asphyxial response being less than its individual components. 7. The amplitudes and shapes of the oscillations in response to 4 s PCO2 alternations were not affected by changing either the steady-background PO2 or PCO2, but the amplitudes of the oscillations to pure PO2 alternations were enhanced by hypoxia and by hypercapnia. The importance of PO2 and PCO2 in giving rise to the natural respiratory oscillations in chemoreceptor discharge depends on the mean levels of the two gases. In normocapnic hypoxia (PO2 ca. 50 Torr) they are equally important but when PO2 is raised it becomes less important.

Action Potentials↗

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.

Animals↗

Role of voltage-dependent calcium channels in stimulus-secretion coupling in rabbit carotid body chemoreceptor cells.

We have defined Ca2+ channel subtypes expressed in rabbit carotid body (CB) chemoreceptor cells and their participation in the stimulus-evoked catecholamine (CA) release. Ca2+ currents (I(Ca)) activated at -30 mV, peaked at +10 mV and were fully blocked by 200 microm Cd2+. L-type channels (sensitive to 2 microm nisoldipine) activated at -30 mV and carried 21 +/- 2% of total I(Ca). Non-L-type channels activated at potentials positive to -10 mV and carried: N channels (sensitive to 1 microM omega-conotoxin-GVIA) 16 +/- 1% of total I(Ca), P/Q channels (sensitive to 3 microM omega-conotoxin-MVIIC after nisoldipine plus GVIA) 23 +/- 3% of total I(Ca) and R channels (resistant to all blockers combined) 40 +/- 3% of total I(Ca). CA release induced by hypoxia, hypercapnic acidosis, dinitrophenol (DNP) and high K(+)(o) in the intact CB was inhibited by 79-98% by 200 microm Cd2+. Hypoxia, hypercapnic acidosis and DNP, depolarized chemoreceptor cells and eventually generated repetitive action potential discharge. Nisoldipine plus MVIIC nearly abolished the release of CAs induced by hypoxia and hypercapnic acidosis and reduced by 74% that induced by DNP. All these secretory responses were insensitive to GVIA. 30 and 100 mm K(+)(o) brought resting membrane potential (E(m)) of chemoreceptor cells (-48.1 +/- 1.2 mV) to -22.5 and +7.2 mV, respectively. Thirty millimolar K(+)(o)-evoked release was abolished by nisoldipine but that induced by 100 mm K(+)(o) was mediated by activation of L, N, and P/Q channels. Data show that tested stimuli depolarize rabbit CB chemoreceptor cells and elicit CA release through Ca2+ entry via voltage-activated channels. Only L and P/Q channels are tightly coupled to the secretion of CA.

Acidosis↗

Modulation of synaptic transmission to second-order peripheral chemoreceptor neurons in caudal nucleus tractus solitarius by alpha1-adrenoreceptors.

Norepinephrine (NE) is an important neurotransmitter in central autonomic regulation. Peripheral chemoreceptor stimulation activates central noradrenergic structures. These structures innervate and therefore could modulate neurons in caudal nucleus tractus solitarius (cNTS), which receives the first central projections from peripheral chemoreceptors. However, the role of alpha(1)-adrenoreceptors in synaptic transmission of peripheral chemoreceptor inputs in cNTS is unknown. We investigated the responses to activation of alpha(1)-adrenoreceptors on glutamatergic and GABAergic inputs in NTS slices using whole-cell recording. Second-order neurons were identified by 1,1'-dilinoleyl-3,3,3',3'-tetra-methylindocarbocyanine, 4-chlorobenzenesulphonate (DiA) labeling of carotid bodies. Electrical stimulation of ipsilateral tractus solitarius was used to evoke excitatory postsynaptic currents (eEPSCs), whereas inhibitory postsynaptic currents were evoked (eIPSCs) by electrically stimulating NTS near the recorded neuron. Application of alpha(1)-adrenoreceptor agonist phenylephrine (PE) at 20 microM significantly decreased amplitudes of eEPSCs (78 +/- 1% of control; n = 16; p < 0.01), and it increased amplitudes of eIPSCs (120 +/- 13% of control; n = 7; p < 0.01). Both effects were blocked by the alpha(1)-adrenoreceptor antagonist prazosin at 10 microM. PE did not change holding current, input resistance, and current-voltage relationship in cNTS neurons. PE significantly changed paired pulse ratios of eEPSC/eIPSCs, increased the frequency of miniature IPSCs (329 +/- 10% of control; n = 6; p < 0.05), but it decreased that of miniature EPSCs (69 +/- 6% of control; n = 5; p < 0.01). PE-induced inhibition of eEPSCs was independent of N-methyl-D-aspartate or GABA(B) receptors. These results suggest that activation of alpha(1)-adrenoreceptors reduces excitatory and enhances inhibitory inputs to second-order peripheral chemoreceptor neurons in cNTS via a presynaptic mechanism. These actions result in the inhibition of synaptic transmission and could play a role in the autonomic responses to hypoxia.

Animals↗

Analysis of chimeric chemoreceptors in Bacillus subtilis reveals a role for CheD in the function of the McpC HAMP domain.

Motile prokaryotes use a sensory circuit for control of the motility apparatus in which ligand-responsive chemoreceptors regulate phosphoryl flux through a modified two-component signal transduction system. The chemoreceptors exhibit a modular architecture, comprising an N-terminal sensory module, a C-terminal output module, and a HAMP domain that connects the N- and C-terminal modules and transmits sensory information between them via an unknown mechanism. The sensory circuits mediated by two chemoreceptors of Bacillus subtilis have been studied in detail. McpB is known to regulate chemotaxis towards the attractant asparagine in a CheD-independent manner, whereas McpC requires CheD to regulate chemotaxis towards the attractant proline. Although CheD is a phylogenetically widespread chemotaxis protein, there exists only a limited understanding of its function. We have constructed chimeras between McpB and McpC to probe the role of CheD in facilitating sensory transduction by McpC. We found that McpC can be converted to a CheD-independent receptor by the replacement of one-half of its HAMP domain with the corresponding sequence from McpB, suggesting that McpC HAMP domain function is complex and may require intermolecular interactions with the CheD protein. When considered in combination with the previous observation that CheD catalyzes covalent modification of the C-terminal modules of B. subtilis receptors, these results suggest that CheD may interact with chemoreceptors at multiple, functionally distinct sites.

Amino Acid Sequence↗

Aminophylline and increased activity of peripheral chemoreceptors in newborn infants.

Peripheral chemoreceptor activity was studied in nine healthy, unsedated neonates (with a mean (SD) postconceptional age of 39 (2) weeks and birth weight of 3000 (400) g) by measuring the inhibition of ventilation elicited by five breaths of 100% oxygen (Dejours technique). Changes in tidal volume, frequency, and minute ventilation were measured before and after administration of aminophylline (10 mg/kg by mouth). Before aminophylline hyperoxia induced a decrease in minute ventilation (from a mean (SE) of 825 (55) to 520 (30) ml/kg/min) as result of reduction of tidal volume (from 12 (0.3) to 8 (0.3) ml/kg). After aminophylline administration the hyperoxia induced decrease in tidal volume (from 14 (0.7) to 6 (0.3) ml/kg) and minute ventilation (from 847 (57) to 386 (21) ml/kg/min) was significantly greater than before. It is concluded that in neonates peripheral chemoreceptors are more active in the presence of aminophylline. It is speculated that aminophylline increases the activity of peripheral chemoreceptors, reducing the breakdown of cAMP, which is a crucial mediator for peripheral chemoreceptor discharge.

Aminophylline↗

Nature of the interaction between central and peripheral chemoreceptor drives in human subjects.

The purpose of the current study was to investigate the nature of the interaction between the central and peripheral chemoreflex loops in humans, using the different speeds of response of the central and peripheral chemoreceptors to enable a temporal separation of their chemical stimulation. Subjects were exposed to an end-tidal Pco2 of 8-10 torr (1 torr = 1 mmHg = 133.3 Pa) above resting Pco2, with end-tidal Po2 = 100 torr, for 8 min. Thirty seconds after the hypercapnic stimulus was withdrawn, a 5-min hypoxic stimulus (end-tidal Po2 = 50 torr) was introduced. The 30-s interval was believed to be sufficient time for the peripheral chemoreceptors to adapt to the new level of carbon dioxide. Over the subsequent 5 min of hypoxia, however, the central chemoreceptors were exposed to diminishing hypercapnia. The response to the hypoxic step was compared with the effect of the same hypoxic step without the preceding period of hypercapnia. In 4 of the 5 subjects studied, the ventilatory response to hypoxia was unaffected by relative hypercapnia at the central chemoreceptor, suggesting that the central and peripheral chemoreflexes were independent of each other.

Adult↗

NADPH oxidase inhibition does not interfere with low PO2 transduction in rat and rabbit CB chemoreceptor cells.

The aim of the present work was to elucidate the role of NADPH oxidase in hypoxia sensing and transduction in the carotid body (CB) chemoreceptor cells. We have studied the effects of several inhibitors of NADPH oxidase on the normoxic and hypoxia-induced release of [3H]catecholamines (CA) in an in vitro preparation of intact CB of the rat and rabbit whose CA deposits have been labeled by prior incubation with the natural precursor [3H]tyrosine. It was found that diphenyleneiodonium (DPI; 0.2-25 microM), an inhibitor of NADPH oxidase, caused a dose-dependent release of [3H]CA from normoxic CB chemoreceptor cells. Contrary to hypoxia, DPI-evoked release was only partially Ca2+ dependent. Concentrations of DPI reported to produce full inhibition of NADPH oxidase in the rat CB did not prevent the hypoxic release response in the rat and rabbit CB chemoreceptor cells, as stimulation with hypoxia in the presence of DPI elicited a response equaling the sum of that produced by DPI and hypoxia applied separately. Neopterin (3-300 microM) and phenylarsine oxide (0.5-2 microM), other inhibitors of NADPH oxidase, did not promote release of [3H]CA in normoxic conditions or affect the response elicited by hypoxia. On the basis of effects of neopterin and phenylarsine oxide, it is concluded that NADPH oxidase does not appear to play a role in oxygen sensing or transduction in the rat and rabbit CB chemoreceptor cells in vitro and, in the context of the present study, that DPI effects are not related to NADPH oxidase inhibition.

Animals↗

Carotid chemoreceptor reflex parasympathetic coronary vasodilation in the dog.

The hypothesis that carotid body chemoreceptor activation with hypoxic-hypercapnic blood elicits reflex coronary vasodilation was investigated. Circumflex or anterior descending coronary artery blood flow was measured in alpha-chloralose-anesthetized, closed-chest dogs. To minimize changes in cardiac metabolism, the heart was paced at a constant rate after atrioventricular heart block, propranolol (1 mg/kg) was given to prevent beta-receptor-mediated alterations in cardiac contractility, and aortic blood pressure was stabilized by means of a blood reservoir. The carotid body regions were vascularly isolated and perfused at constant pressure with arterial blood or hypoxic-hypercapnic blood. Under these conditions, carotid body chemoreceptor stimulation with hypoxic or hypoxic-hypercapnic blood for 90 s produced atrial bradycardia and a transient increase in coronary blood flow of 36-53% above prestimulation values. The augmented coronary flow was accompanied by a transient increase in coronary sinus O2 tension of 4.6-5.7 mmHg. Aortic blood pressure varied less than 10 mmHg. Intracarotid injections of nicotine (0.1 microgram/kg) or cyanide (150 micrograms) produced similar results. The coronary response to chemoreceptor stimulation with hypoxic blood or drugs was abolished when the reflex arc was interrupted with atropine (0.5 mg/kg). It is concluded that transient reflex parasympathetic coronary vasodilation is elicited by hypoxic or hypoxic-hypercapnic stimulation of carotid body chemoreceptors.

Animals↗

Cardiovascular responses to nasal water flow in rats are unaffected by chemoreceptor drive.

Peripheral chemoreceptors generally play a limited role in the initial development of diving bradycardia in mammals. However, T.F. Huang and Y.I. Peng (Jpn. J. Physiol. 26: 395-401, 1976) reported that peripheral chemoreceptors are very important for manifestation of the diving response in conscious rats. The objectives of this study were to reinvestigate those findings and determine whether the cardiovascular responses to simulated diving in the rat were potentiated during preexisting hypoxia or hypercapnia. Responses to simulated diving were elicited by nasal water flow with concurrent apnea in paralyzed, artificially ventilated Sprague-Dawley rats anesthetized with Innovar. The experiments show that nasal stimulation in the rat results in rapid bradycardia and hypotension and that these responses are not due to laryngeal stimulation. The data also suggest that chemoreceptors do not play a role in the initiation of the responses to simulated diving in rats and that preexisting chemoreceptor drive does not alter the cardiovascular responses. Additionally, we found that concomitant expiratory apnea is necessary to sustain the profound initial cardiovascular changes induced by nasal water flow.

Animals↗