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A negative interaction between brainstem and peripheral respiratory chemoreceptors modulates peripheral chemoreflex magnitude
Author(s) -
Day Trevor A.,
Wilson Richard J. A.
Publication year - 2009
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2008.160689
Subject(s) - brainstem , carotid body , peripheral chemoreceptors , chemoreceptor , peripheral , respiratory system , hypoxia (environmental) , central chemoreceptors , neuroscience , control of respiration , medicine , endocrinology , biology , anesthesia , electrophysiology , chemistry , oxygen , receptor , organic chemistry
Interaction between central (brainstem) and peripheral (carotid body) respiratory chemosensitivity is vital to protect blood gases against potentially deleterious fluctuations, especially during sleep. Previously, using an in situ arterially perfused, vagotomized, decerebrate preparation in which brainstem and peripheral chemoreceptors are perfused separately (i.e. dual perfused preparation; DPP), we observed that the phrenic response to specific carotid body hypoxia was larger when the brainstem was held at 25 Torr P CO 2compared to 50 Torr P CO 2. This suggests a negative (i.e. hypo‐additive) interaction between chemoreceptors. The current study was designed to (a) determine whether this observation could be generalized to all carotid body stimuli, and (b) exclude the possibility that the hypo‐additive response was the simple consequence of ventilatory saturation at high brainstem P CO 2. Specifically, we tested how steady‐state brainstem P CO 2modulates peripheral chemoreflex magnitude in response to carotid body P CO 2and P O 2perturbations, both above and below eupnoeic levels. We found that the peripheral chemoreflex was more responsive the lower the brainstem P CO 2regardless of whether the peripheral chemoreceptors received stimuli which increased or decreased activation. These findings demonstrate a negative interaction between brainstem and peripheral chemosensitivity in the rat in the absence of ventilatory saturation. We suggest that a negative interaction in humans may contribute to increased controller gain associated with sleep‐related breathing disorders and propose that the assumption of simple addition between chemoreceptor inputs used in current models of the respiratory control system be reconsidered.