The Carotid Chemoreceptors are a Major Determinant of Ventilatory CO2 Sensitivity and of PaCO2 During Eupneic Breathing

Forster, H. V.; Martino, Paul; Hodges, Matt; Krause, Katie; Bonis, Joshua M.; Davis, Suzanne E.; Pan, Lawrence

doi:10.1007/978-0-387-73693-8_56

Cited by 40 publications

(35 citation statements)

References 19 publications

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“…CBs contribute greatly to resting ventilation, even in normoxia (Olson et al, 1988;Forster et al, 2008;. Although hyperoxia silences the CBs, ventilation is barely decreased in rats (present results;Olson et al, 1988) or mildly stimulated in humans (Becker et al, 1996;Ainslie and Duffin, 2009;Chowdhuri et al, 2010).…”

Section: Cb Stimulation Can Activate F R Via Pathways That Bypass Rtnsupporting

confidence: 46%

Hypoxia Silences Retrotrapezoid Nucleus Respiratory Chemoreceptors via Alkalosis

et al. 2015

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In conscious mammals, hypoxia or hypercapnia stimulates breathing while theoretically exerting opposite effects on central respiratory chemoreceptors (CRCs). We tested this theory by examining how hypoxia and hypercapnia change the activity of the retrotrapezoid nucleus (RTN), a putative CRC and chemoreflex integrator. Archaerhodopsin-(Arch)-transduced RTN neurons were reversibly silenced by light in anesthetized rats. We bilaterally transduced RTN and nearby C1 neurons with Arch (PRSx8-ArchT-EYFP-LVV) and measured the cardiorespiratory consequences of Arch activation (10 s) in conscious rats during normoxia, hypoxia, or hyperoxia. RTN photoinhibition reduced breathing equally during non-REM sleep and quiet wake. Compared with normoxia, the breathing frequency reduction (⌬f R ) was larger in hyperoxia (65% FiO 2 ), smaller in 15% FiO 2 , and absent in 12% FiO 2 . Tidal volume changes (⌬V T ) followed the same trend. The effect of hypoxia on ⌬f R was not arousal-dependent but was reversed by reacidifying the blood (acetazolamide; 3% FiCO 2 ). ⌬f R was highly correlated with arterial pH up to arterial pH (pHa) 7.5 with no frequency inhibition occurring above pHa 7.53. Blood pressure was minimally reduced suggesting that C1 neurons were very modestly inhibited. In conclusion, RTN neurons regulate eupneic breathing about equally during both sleep and wake. RTN neurons are the first putative CRCs demonstrably silenced by hypocapnic hypoxia in conscious mammals. RTN neurons are silent above pHa 7.5 and increasingly active below this value. During hyperoxia, RTN activation maintains breathing despite the inactivity of the carotid bodies. Finally, during hypocapnic hypoxia, carotid body stimulation increases breathing frequency via pathways that bypass RTN.

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Section: Cb Stimulation Can Activate F R Via Pathways That Bypass Rtnsupporting

confidence: 46%

Hypoxia Silences Retrotrapezoid Nucleus Respiratory Chemoreceptors via Alkalosis

et al. 2015

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“…However, their contribution to the overall ventilatory CO 2 sensitivity has been somehow undeservedly neglected, largely owing to the well-known fact that strong ventilatory responses to CO 2 are usually preserved in animals with denervated peripheral chemoreceptors (see, Heeringa et al 1979). Recent evidence suggests that the carotid chemoreceptors contribute about one-third of the overall response to CO 2 challenge and play an even more significant role in controlling arterial PCO 2 during eupneic breathing (Forster et al 2008).…”

Section: Peripheral Chemosensory Inputsmentioning

confidence: 99%

Chemosensory pathways in the brainstem controlling cardiorespiratory activity

Spyer

Gourine

2009

Phil. Trans. R. Soc. B

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Cardiorespiratory activity is controlled by a network of neurons located within the lower brainstem. The basic rhythm of breathing is generated by neuronal circuits within the medullary pre-Bö tzinger complex, modulated by pontine and other inputs from cell groups within the medulla oblongata and then transmitted to bulbospinal pre-motor neurons that relay the respiratory pattern to cranial and spinal motor neurons controlling respiratory muscles. Cardiovascular sympathetic and vagal activities have characteristic discharges that are patterned by respiratory activity. This patterning ensures ventilation-perfusion matching for optimal respiratory gas exchange within the lungs. Peripheral arterial chemoreceptors and central respiratory chemoreceptors are crucial for the maintenance of cardiorespiratory homeostasis. Inputs from these receptors ensure adaptive changes in the respiratory and cardiovascular motor outputs in various environmental and physiological conditions. Many of the connections in the reflex pathway that mediates the peripheral arterial chemoreceptor input have been established. The nucleus tractus solitarii, the ventral respiratory network, presympathetic circuitry and vagal pre-ganglionic neurons at the level of the medulla oblongata are integral components, although supramedullary structures also play a role in patterning autonomic outflows according to behavioural requirements. These medullary structures mediate cardiorespiratory reflexes that are initiated by the carotid and aortic bodies in response to acute changes in PO 2 , PCO 2 and pH in the arterial blood. The level of arterial PCO 2 is the primary factor in determining respiratory drive and although there is a significant role of the arterial chemoreceptors, the principal sensor is located either at or in close proximity to the ventral surface of the medulla. The cellular and molecular mechanisms of central chemosensitivity as well as the neural basis for the integration of central and peripheral chemosensory inputs within the medulla remain challenging issues, but ones that have some emerging answers.

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“…Zakynthinos et al [15], however, did not ruled out the possibility that the CBs can be involved in generation of HCVR under conditions of breathing of a gas mixture containing increased amounts of O 2 . There are reports that denervation of the CBs leads to a greater tolerance of central chemoreceptors with respect to hypercapnic acidosis [16]. Suppression of the response of the respiratory system to hypoxic stimulation observed at aging [4,5] can be considered a proof of the existence of some age-related physiological "denervation/ desensitization" of the CBs, i.e., a noticeable drop in their activity within the above ontogenesis phase.…”

Section: Resultsmentioning

confidence: 98%

Aging-related changes in the sensitivity of the system of respiratory control and the intensity of free-radical processes in humans

Колесникова

2008

Neurophysiology

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Results of a comparative study of the sensitivity of the system of respiratory control to increases in the СО 2 concentration and the intensity of free-radical processes in young and elderly subjects are described. It is shown that normal (natural) aging is accompanied by a decrease in the sensitivity of the respiratory system to hypercapnic stimulation and a parallel significant decrease in the activity of catalase in the blood of examined subjects. Mechanisms responsible for the modifications of the sensitivity of the system of respiratory control to hypercapnia are discussed; these shifts can be at least partly related to changes in the intensity of production of free radicals observed in elderly subjects.

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The Carotid Chemoreceptors are a Major Determinant of Ventilatory CO2 Sensitivity and of PaCO2 During Eupneic Breathing

Cited by 40 publications

References 19 publications

Hypoxia Silences Retrotrapezoid Nucleus Respiratory Chemoreceptors via Alkalosis

Hypoxia Silences Retrotrapezoid Nucleus Respiratory Chemoreceptors via Alkalosis

Chemosensory pathways in the brainstem controlling cardiorespiratory activity

Aging-related changes in the sensitivity of the system of respiratory control and the intensity of free-radical processes in humans

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