Respiratory Reflexes Research Articles

Morphological Development and Expression of Neurotrophin Receptors in the Laryngeal Sensory Corpuscles

Morphological development of sensory structures in the laryngeal mucosa of postnatal rats was observed by use of immunohistochemistry for protein gene-product 9.5 (PGP9.5). Moreover, expression changes of high affinity neurotrophin receptors, TrkA, TrkB and TrkC, and low affinity neurotrophin receptor p75(NTR) were examined to elucidate the relationship to morphogenesis. Intraepithelial nerve endings and parent axons of the laminar endings with immunoreactivity for PGP9.5 have already appeared in the rat on embryonic day 18 (E18) as well as solitary chemoreceptor cells in the glottic cleft. According to neurotrophin receptors, TrkA immunoreactivity were observed on and after postnatal week 3 (3W) in the nervous sensory structures, that is, free nerve endings, laminar endings and sub- and intragemmal plexuses of the taste buds. In the laminar endings, TrkC immunoreactivity was also observed on and after 3W. According to the laryngeal sensory cells, the solitary chemoreceptor cells were immunoreactive to TrkA, TrkB, and TrkC on and after postnatal day 3 (P3). In the taste buds in arytenoid region, taste cells were immunoreactive for TrkA, TrkB, and TrkC on and after 3W, P14, and 3W, respectively. Immunoreactivity for p75(NTR) was observed on the surface of taste cells on and after P9. The results of the present study suggest that sensory structures in the laryngeal mucosa were developed on perinatal days to involve respiratory reflex, and that neurotrophin receptors may take part in the regulation and maintenance of sensory structures.

Breath‐taking complexity of vagal C‐fibre nociceptors: implications for inflammatory pulmonary disease, dyspnoea and cough

Breath‐taking complexity of vagal C‐fibre nociceptors: implications for inflammatory pulmonary disease, dyspnoea and cough

Respiration drives phase synchronization between blood pressure and RR interval following loss of cardiovagal baroreflex during vasovagal syncope

Loss of the cardiovagal baroreflex (CVB), thoracic hypovolemia, and hyperpnea contribute to the nonlinear time-dependent hemodynamic instability of vasovagal syncope. We used a nonlinear phase synchronization index (PhSI) to describe the extent of coupling between cardiorespiratory parameters, systolic blood pressure (SBP) or arterial pressure (AP), RR interval (RR), and ventilation, and a directional index (DI) measuring the direction of coupling. We also examined phase differences directly. We hypothesized that AP-RR interval PhSI would be normal during early upright tilt, indicating intact CVB, but would progressively decrease as faint approached and CVB failed. Continuous measurements of AP, RR interval, respiratory plethysomography, and end-tidal CO2 were recorded supine and during 70-degree head-up tilt in 15 control subjects and 15 fainters. Data were evaluated during five distinct times: baseline, early tilt, late tilt, faint, and recovery. During late tilt to faint, fainters exhibited a biphasic change in SBP-RR interval PhSI. Initially in fainters during late tilt, SBP-RR interval PhSI decreased (fainters, from 0.65±0.04 to 0.24±0.03 vs. control subjects, from 0.51±0.03 to 0.48±0.03; P<0.01) but then increased at the time of faint (fainters=0.80±0.03 vs. control subjects=0.42±0.04; P<0.001) coinciding with a change in phase difference from positive to negative. Starting in late tilt and continuing through faint, fainters exhibited increasing phase coupling between respiration and AP PhSI (fainters=0.54±0.06 vs. control subjects=0.27±0.03; P<0.001) and between respiration and RR interval (fainters=0.54±0.05 vs. control subjects=0.37±0.04; P<0.01). DI indicated respiratory driven AP (fainters=0.84±0.04 vs. control subjects=0.39±0.09; P<0.01) and RR interval (fainters=0.73±0.10 vs. control subjects=0.23±0.11; P<0.001) in fainters. The initial drop in the SBP-RR interval PhSI and directional change of phase difference at late tilt indicates loss of cardiovagal baroreflex. The subsequent increase in SBP-RR interval PhSI is due to a respiratory synchronization and drive on both AP and RR interval. Cardiovagal baroreflex is lost before syncope and supplanted by respiratory reflexes, producing hypotension and bradycardia.

Influence of codeine on lobeline-induced respiratory reflexes and sensations and on ventilation with exercise in healthy subjects

In 15 healthy subjects, the effect of 60 mg oral codeine and placebo was examined on intravenously injected lobeline-elicited respiratory reflexes and sensations. Its influence was also studied on ventilation and appearance of distressful respiratory sensations with modest but incremental exercise. After placebo, tachypnoea and respiratory sensations were evoked with 12.1 ± 1.9 μg/kg of lobeline i.v. (mean threshold dose) and after codeine, by significantly higher doses i.e., 18.0 ± 3.1 μg/kg (P < 0.05). Additionally after codeine, in response to incremental doses of lobeline the respiratory reflex was notably attenuated and the magnitude of respiratory sensations, subdued. Dry cough seen in 66% of the subjects with suprathreshold doses of lobeline i.e., 22.0 ± 3.4 μg/kg (mean), appeared post codeine, with significantly higher doses i.e., 27.0 ± 3.9 μg/kg (mean) (P < 0.05) and in a fewer subjects (60%). Mean increase in minute ventilation at the end of 8 min of incremental treadmill walking after codeine was 21% less than after placebo (P < 0.05); 60% of the subjects continued to walk for an additional 4 min and the onset of respiratory discomfort was delayed by 1-5 min. This is the first report of an attenuation of lobeline-elicited respiratory reflexes and sensations that are attributable to J receptors (pulmonary C fibres) by a pharmacological entity. It also suggests that codeine decreased these receptors' known contribution to respiratory augmentation and motor inhibition during exercise, which was seen as a delay in the onset of, and a decrease in the magnitude of respiratory discomfort during treadmill walking and an increase in the duration walked by more than half the subjects.

Eficácia do sistema de contenção (automatizado e mecânico) no atordoamento de bovinos

Um total de 800 bovinos machos (nelore/anelorados), com idade entre 28 e 36 meses, foi atordoado com pistola pneumática, com pressão de operação de 11 a 12bar e haste de penetração de 15.9mm de diâmetro, em sistemas de contenção diferentes (mecânico e atomatizado). O box de contenção mecânico tradicional (2,53x0,88x2,20m) não permitiu a contenção da cabeça do animal; no segundo tratamento utilizou-se box de contenção automatizado (2,60x0,85x2,30m), com parede lateral e piso móveis, guilhotina e elevador de cabeça. O box automatizado proporcionou menor número de disparos necessários para o atordoamento (1,0625±0,013) em comparação ao mecânico(1,2025±0,026), (P≤0,0001), reduziu a distância em relação ao ponto ideal no primeiro disparo (1,246±0,918 e 2,357±1,246) e no segundo (3,042±0,141 e 4,016±0,101), (P 0,0001), assim como proporcionou ausência de reflexo respiratório comparativamente ao sistema mecânico (0,0275±0,008), (P≤0,001). O box automatizado apresentou maior bem-estar e maior eficácia na contenção e insensibilização dos bovinos

Evaluation of newborn canine viability by means of umbilical vein lactate measurement, apgar score and uterine tocodynamometry

Newborn viability evaluation and early detection of fetal distress could contribute to reducing mortality at birth in canine species. High neonatal mortality rate in dogs is reported subsequent to complicated or uncomplicated whelping. Umbilical vein lactate and tocodynamometry could provide valuable clinical information to the obstetricians so that appropriate medical and surgical treatments or oxygen and warm administration can be properly and timely applied to mother and newborn pup. In humans, the fetal lactate level represents an objective indicator of fetal distress and a valid predictor of babies' survival. Fetal acidosis recognition by umbilical lactate (UL) measurement, APGAR score classification, and uterine activity monitoring during labour, can represent an advanced system in the evaluation of the canine newborn patient. The purpose of this study was to correlate UL levels with canine neonatal morbidity and mortality within 48 h of birth. We evaluated the relationship among neonatal parameters at birth (mucous membrane color, heart and respiratory rate, reflex irritability, mobility, suckling and vocalization, UL, weight, and temperature) with labour characteristics (uterine contractions recorded by the tocodynamometric system of Whelpwise™ Veterinary Perinatal Specialties®, delivery time, and pup presentation), in view to predict pup viability. We considered also vaginal parturition versus elective and emergency Caesarean section, and uterotonic drugs influence on delivery. Umbilical lactate concentration proved to be useful to predict canine neonatal mortality within 48 h of birth (P < 0.05). We identified 5 mmol/L of vein umbilical lactate concentration as the cut off value, allowing us to distinguish between healthy and distressed pups. Higher values of UL were related with distressed pups, whereas lower values characterized vigorous pups. Lactate concentrations lower than 5 mmol/L and APGAR scores higher than 9, related to mean delivery time of 105 min with effective uterine contractions (10 mm of Hg of strength or more, frequency from 4 to 12 contractions per hour, and 2–5 min in duration), should be considered good prognostic factors in canine labour and neonatology.

Sensory Detection and Responses to Toxic Gases: Mechanisms, Health Effects, and Countermeasures

The inhalation of reactive gases and vapors can lead to severe damage of the airways and lung, compromising the function of the respiratory system. Exposures to oxidizing, electrophilic, acidic, or basic gases frequently occur in occupational and ambient environments. Corrosive gases and vapors such as chlorine, phosgene, and chloropicrin were used as warfare agents and in terrorist acts. Chemical airway exposures are detected by the olfactory, gustatory, and nociceptive sensory systems that initiate protective physiological and behavioral responses. This review focuses on the role of airway nociceptive sensory neurons in chemical sensing and discusses the recent discovery of neuronal receptors for reactive chemicals. Using physiological, imaging, and genetic approaches, Transient Receptor Potential (TRP) ion channels in sensory neurons were shown to respond to a wide range of noxious chemical stimuli, initiating pain, respiratory depression, cough, glandular secretions, and other protective responses. TRPA1, a TRP ion channel expressed in chemosensory C-fibers, is activated by almost all oxidizing and electrophilic chemicals, including chlorine, acrolein, tear gas agents, and methyl isocyanate, the highly noxious chemical released in the Bhopal disaster. Chemicals likely activate TRPA1 through covalent protein modification. Animal studies using TRPA1 antagonists or TRPA1-deficient mice confirmed the role of TRPA1 in chemically induced respiratory reflexes, pain, and inflammation in vivo. New research shows that sensory neurons are not merely passive sensors of chemical exposures. Sensory channels such as TRPA1 are essential for maintenance of airway inflammation in asthma and may contribute to the progression of airway injury following high-level chemical exposures.

Raphe serotonin neurons: characteristics of central chemoreceptors in situ

The location and identity of central chemoreceptors is debated, and several different neuronal populations may contribute to central chemosensitivity. Rat raphé serotonin (5HT) neurons, intrinsically sensitive to pH change in vitro, are proposed as chemoreceptors in vivo. Characterization of 5HT neurons as chemoreceptors is refuted, as electrophysiological evidence for chemosensitive 5HT neurons is lacking in vivo. We address this controversy using the unanesthetized juvenile rat in situ perfused decerebrate brainstem preparation. This preparation displays respiratory patterns and reflexes comparable to an intact animal. Through extracellular recording in medullary raphe we demonstrate both chemosensitive and insensitive neurons, including cells with firing patterns expected of 5HT neurons. We also report results of extracellular recording combined with juxtacellular labeling of raphe neurons, identifying neurotransmitter phenotypes of sensitive and insensitive cells. Our results support the presence of chemosensitive 5HT neurons in the raphe in situ. Given the intrinsic chemosensitivity of such neurons in vitro, our data support a role for raphe 5HT neurons as central chemoreceptors in vivo. Supported by NIH 2U54NS041069‐06A1

Respiratory and Circulatory Reflexes in Response to Water Stimuli Applied to the Nasal Cavity in Anesthetized Rabbits

Respiratory and Circulatory Reflexes in Response to Water Stimuli Applied to the Nasal Cavity in Anesthetized Rabbits

A streetcar named urge-to-cough

in the Tennessee Williams play A Streetcar Named Desire , we learn that Blanche DuBois is considerably more complex than meets the eye. So too is a recently identified sensation associated with the production of cough, known as the “urge-to-cough” ([3][1], [4][2]). In this issue of the Journal

The effect of bilateral vagal blockade on respiration

Although respiratory regulation has been extensively studied so far, the relation between the vagal nerves and respiratory reflex in man is still open to controversy. This paper describes the effect of bilateral vagal blockade on respiration. 1) Dyspnea due to unilateral bronchial occlusion. This type of dyspnea is caused by extreme depression of the intrabronchial pressure on the occluded side and is accompanied by a rapid increase in respiratory rate and a rapid decrease in tidal volume. This type of dyspnea is relieved by blockade of the ipsilateral cervical vagal nerve. 2) Animal experiments on bilateral lung transplantation, heart-lung transplantation and bilateral cervical vagal blockade. The respiratory changes induced by CO2 inhalation, low O2 inhalation, respiratory stimulant. Loss of blood or fever stimulation in the manipulated dogs were compared with those in normal controls. CO2 inhalation alone produced differences in the respiratory rates and tidal volumes between the two groups. The tidal volume increase under CO2 inhalation was suppressed by the inflation reflex but other afferent vagal nerves seemed to be closely associated with the increased respiratory rate. 3) Vagal nerve reflex in humans. Blockade of the bilateral cervical vagal nerves in an awake state resulted in irregular PETCO2 in cases that had been stable and sometimes produced a pattern of Cheyne-Stokes respiration. Inhalation of 5% CO2 restored the regular rhythm of respiration and enhanced the response to CO2. When subjected to bilateral vagal blockade in an awake state, the patient expressed an unbearbly uneasy dyspneic sensation as if he were pulled into a bottomless abyss. This was demonstrated by the unstable FRC level.

Muscarinic modulation of TASK-like background potassium channel in rat carotid body chemoreceptor cells

The carotid body is the main peripheral arterial chemoreceptor and it is essential to initiate the cardiovascular and respiratory compensatory reflex responses to a decrease in the arterial oxygen. The carotid body chemoreceptor (type-I) cells respond to hypoxia with membrane depolarization, voltage-gated Ca 2+ entry and secretion of transmitters. A key step in this response is the inhibition of a TASK-like background K + current. It has been reported that TASK-K + channels can be modulated by G-protein coupled receptors, such as the muscarinic acetylcholine receptor (mAChRs). Since there is a proposed role for ACh as an autocrine/paracrine modulator of the carotid body function, we have investigated the possible regulation of the background K + current by mAChRs. In identified type-I cells, methacholine (100 µM) or muscarine (50 µM) increased intracellular Ca 2+ levels. In cell-attached patch recordings, TASK-K + background channel activity was reduced by ∼ 50% during mAChR activation and by the diacylglycerol analogue oleoylacetylglycerol (OAG, 20 µM). The co-application of both metacholine and OAG do not further inhibit K + channel activity. In addition, two chemically different inhibitors of protein kinase C activity, calphostin C (100 nM) and chelerythrine (50 µM) are both able to suppress the muscarinic inhibition of the TASK-like K + channel and to increase channel activity in the absence of mAChR agonists. Our results suggest a muscarinic regulation of the TASK-like K + current in rat carotid body type-I cells through a PLC/PKC-dependent pathway. Additionally, our findings are consistent with an autocrine/paracrine role for cholinergic autoreceptors present within the carotid body.

Cardiovascular and respiratory reflexes of the gulf toadfish (Opsanus beta) during acute hypoxia

The acute cardiovascular and respiratory responses of the gulf toadfish, Opsanus beta, to acute hypoxia or exposure to the O(2) chemoreceptor stimulant, sodium cyanide (NaCN) were characterized and the role of serotonin type 2 (5-HT(2)) receptors in mediating these responses was investigated. Toadfish responded to hypoxia or NaCN exposure with a decrease in heart rate (fH) and an increase in breathing amplitude (V(AMP)) but no change in breathing frequency (fR). The bradycardia appeared to be mediated to some extent by 5-HT(2) receptors, as methysergide, a non-selective 5-HT(1/2) receptor antagonist, and ketanserin, a 5-HT(2) receptor antagonist, attenuated the response. Injection of alpha-methyl-5-HT, a 5-HT(2) agonist, also resulted in bradycardia that was inhibited by ketanserin, lending further support for 5-HT(2) receptor involvement, possibly 5-HT(2A) or 5-HT(2C), in the regulation of fH. External NaCN exposure resulted in a significant decrease in caudal arterial blood pressure (P(CA)) that was attenuated by methysergide. In contrast, injection with alpha-methyl-5-HT resulted in a substantial increase in P(CA) that was not affected by ketanserin, suggesting the possible involvement of 5-HT(2B) or 5-HT(2C) receptors. These data are the first to suggest a unique distribution of 5-HT(2B/2C) receptors may be involved in mediating vasoconstriction of the systemic vasculature of toadfish. These data also provide mechanistic support for why pulsatile urea excretion, believed to be regulated by 5-HT via the toadfish 5-HT(2A) receptor, is not triggered by hypoxia or external chemoreceptor activation.

Galanin microinjection into the PreBötzinger or the Bötzinger Complex terminates central inspiratory activity and reduces responses to hypoxia and hypercapnia in rat

Respiratory rhythm is generated and shaped by the synaptic interaction of neurons in the Bötzinger Complex (BötC) and PreBötzinger Complex (PreBötC) located in the ventral respiratory column of the medulla. Metabotropic receptors are important modulators of fast neurotransmission in the generation and shaping of respiratory rhythm. Microinjection of the neuropeptide galanin (1mM, 50 nL, 50 pmol) into functionally identified BötC or PreBötC in urethane anesthetized, mechanically ventilated and vagotomized rats caused severe dysrhythmia or persistent apnea. In the BötC and PreBötC, galanin reduced the ventilatory response to hypercapnia (5% CO(2)) by 21% (P<0.001) and 38% (P<0.01) respectively. In the BötC and PreBötC, galanin reduced the ventilatory response to hypoxia (10% O(2)) by 15% (P<0.05) and 23% (P<0.01) respectively. These results indicate that microinjection of galanin into the BötC or PreBötC depresses a neural substrate required for the generation of respiratory motor output and reflex responses to hypercapnea and hypoxia.

Discharge rate profiles of paratrigeminal nucleus neurons throughout a pressor event in non-anaesthetized rats

Located in the lower brainstem, the paratrigeminal nucleus (Pa5) is related to cardiorespiratory autonomic reflex functions. To characterize the structures' role in blood pressure regulation and the cardiovascular reflex responses Pa5 unit activity was evaluated during a phenylephrine-produced pressor response in non-anaesthetized rats by means of simultaneous many-unit recording. Ninety five percent of the identified Pa5 responded to baroreceptor stimulation, 77% increasing and 23% decreasing firing rates. Cross-correlation analysis of neuron electrical behavior referenced to the heart beat event revealed that 65% of the featured cardiac cycle-locked rhythmic activity. The identification of neurons that change firing rates in response to increases of arterial pressure with cardiac cycle-locked rhythmic activity, further supports for a role for the nucleus in moment to moment control of blood pressure. The largest changes in firing rate occurred in the units with low resting firing rates in response to the ascending phase of the pressor event. Thus, the group displaying both cardiac cycle-locked and other rhythmic activities within the ranges of cardiac and respiratory rates or arterial pressure low frequencies, is probably the most influential regarding homoeostatic reflex responses. The findings advance the notion that the dynamic control of blood pressure involves lower brainstem integration of cardiac and respiratory reflexes.

Transient Receptor Potential Ankyrin 1 Mediates Toluene Diisocyanate–Evoked Respiratory Irritation

Toluene diisocyanate (TDI), a reactive, hazardous irritant, causes respiratory symptoms such as cough, rhinitis, dyspnea, and chest tightness in exposed workers. Although previous animal studies have shown that TDI causes respiratory reflexes that are abolished by desensitization of capsaicin-sensitive sensory nerves, the specific molecular identity of the transducer(s) responsible for sensing this noxious stimulus has, to date, remained elusive. Recent studies have demonstrated that transient receptor potential ankyrin 1 (TRPA1), an ion channel largely restricted to a subset of capsaicin-sensitive sensory nerves, functions as a transducer capable of initiating reflex responses to many reactive chemical stimuli. We therefore hypothesized that TRPA1 is the primary molecular transducer through which TDI causes sensory nerve activation and respiratory reflexes. Consistent with this hypothesis, TDI activated TRPA1, but not the capsaicin-sensitive transient receptor potential vanilloid 1 channel, in heterologous expression systems. TDI also activated a subset of dissociated trigeminal sensory neurons from wild-type but not TRPA1-deficient mice. In vivo, TDI mimicked known TRPA1 agonists by causing a pronounced decrease in breathing rate, indicative of respiratory sensory irritation, and this reflex was abolished in TRPA1-deficient mice. Together, our data suggest that TDI causes sensory nerve activation and airway sensory irritation via the activation of the ion channel, TRPA1.

Local antagonism of intertrigeminal region metabotropic glutamate receptors exacerbates apneic responses to intravenous serotonin.

Injections of a broad spectrum glutamate receptor antagonist into the pontine intertrigeminal region (ITR) exacerbate vagal reflex apnea produced by intravenous serotonin infusion. This effect is not reproduced by ITR injections with either NMDA or AMPA receptor antagonists. Here, we tested the hypothesis that ITR injection with a metabotropic glutamate antagonist would alter respiratory responses to serotonin (5-HT) intravenous infusions. In anesthetized adult male rats (N=20; Sprague-Dawley) AIDA (1-aminoindan-1,5-dicarboxylic acid), a specific antagonist of the type 1 metabotropic glutamate receptor (mGlu1R), was microinjected unilaterally into the ITR to block 5-HT evoked apnea. Respiratory pattern changes evoked by ITR-glutamate injection and by intravenous serotonin (5-HT) infusion (0.5 microl, 0.05 M; or 2.5x10(-8) mol) were characterized according to apnea expression and duration, as well as coefficients of variation for breath duration (CVTT) and amplitude (CVVT) before and after ITR AIDA injection. Unilateral AIDA blockade of the ITR significantly increased the duration of apnea evoked by 5-HT infusion (p<0.03 for each dose tested) during the 30s following infusion in a dose-dependent fashion, with the two highest doses resulting in intermittent apneas for at least 10 min following a bolus 5-HT infusion. Similar prolonged increases in CVTT and CVVT with respect to control were associated with ITR AIDA injections. These findings suggest that brief perturbations of vagal afferent pathways can produce ongoing respiratory dysrhythmia, including spontaneous apnea, and that glutamatergic neurotransmission within ITR may be important for damping such disturbances. The present observations also suggest that such respiratory damping may be mediated by mGlu1 receptors. These findings extend our understanding of the role of the intertrigeminal region in modulating respiratory reflexes.

Rapidly adapting receptors in acute heart failure and their impact on dyspnea

Acute heart failure is associated with dyspnea that is usually defined as difficulty in breathing that is accompanied by an element of distress. It is commonly associated with an increase in the rate of ventilation, wheezing, an increase in airway secretions and cough. This review examines the reflexes which generate these responses with particular reference to the role of rapidly adapting receptors (RAR) in the airways. The essential feature of acute heart failure is an increase in pulmonary extravascular fluid volume. Small acute increases in extravascular fluid volume in the airways activate the RAR. With larger increases both the RAR and the C-fiber receptors in the airways and the alveoli are activated. Activation of RAR causes a reflex increase in respiratory rate, tracheal tone and mucus secretion from the airways. It is suggested that the RAR play a significant role in monitoring changes in the extravascular fluid volume of the airways and mediate the respiratory reflexes associated with acute heart failure.

Differential effects of airway afferent nerve subtypes on cough and respiration in anesthetized guinea pigs

The hypothesis that respiratory reflexes, such as cough, reflect the net and often opposing effects of activation of multiple afferent nerve subpopulations throughout the airways was evaluated. Laryngeal and tracheal mucosal challenge with either citric acid or mechanical probing reliably evoked coughing in anesthetized guinea pigs. No other stimulus reliably evoked coughing in these animals, regardless of route of administration and despite some profound effects on respiration. Selectively activating vagal C-fibers arising from the nodose ganglia with either adenosine or 2-methyl-5-HT evoked only tachypnea. Selectively activating vagal afferents arising from the jugular ganglia induced respiratory slowing and apnea. Nasal afferent nerve activation by capsaicin, citric acid, hypertonic saline, or histamine evoked only respiratory slowing. Histamine, which activates intrapulmonary rapidly adapting receptors but not airway or lung C-fibers or tracheal bronchial cough receptors induced bronchospasm and tachypnea, but no coughing. The results indicate that the reflexes initiated by stimuli thought to be selective for some afferent nerve subtypes will likely depend on the net and potentially opposing effects of multiple afferent nerve subpopulations throughout the airways. The data also provide further evidence that the afferent nerves regulating cough in anesthetized guinea pigs are distinct from either C-fibers or intrapulmonary rapidly adapting receptors.

Point:Counterpoint: Respiratory sinus arrhythmia is due to a central mechanism vs. respiratory sinus arrhythmia is due to the baroreflex mechanism

Blood pressure and heart periods fluctuate at respiratory frequencies in healthy humans. Some researchers ([8][1], [23][2]) explain this as a cause-and-effect relation: blood pressure changes trigger baroreflex-mediated R-R interval changes. Here I make the case that respiratory sinus arrhythmia is