Central CO2 chemoreception and integrated neural mechanisms of cardiovascular and respiratory control

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dc.contributor.author Guyenet, Patrice G.
dc.contributor.author Stornetta, Ruth L.
dc.contributor.author Abbott, Stephen B.G.
dc.contributor.author Depuy, Seth D.
dc.contributor.author Fortuna, Michal G.
dc.contributor.author Kanbar, Roy
dc.date.accessioned 2016-10-10T10:22:25Z
dc.date.available 2016-10-10T10:22:25Z
dc.date.copyright 2010 en_US
dc.date.issued 2016-10-10
dc.identifier.issn 8750-7587 en_US
dc.identifier.uri http://hdl.handle.net/10725/4545
dc.description.abstract In this review, we examine why blood pressure (BP) and sympathetic nerve activity (SNA) increase during a rise in central nervous system (CNS) Pco2 (central chemoreceptor stimulation). CNS acidification modifies SNA by two classes of mechanisms. The first one depends on the activation of the central respiratory controller (CRG) and causes the much-emphasized respiratory modulation of the SNA. The CRG probably modulates SNA at several brain stem or spinal locations, but the most important site of interaction seems to be the caudal ventrolateral medulla (CVLM), where unidentified components of the CRG periodically gate the baroreflex. CNS Pco2 also influences sympathetic tone in a CRG-independent manner, and we propose that this process operates differently according to the level of CNS Pco2. In normocapnia and indeed even below the ventilatory recruitment threshold, CNS Pco2 exerts a tonic concentration-dependent excitatory effect on SNA that is plausibly mediated by specialized brain stem chemoreceptors such as the retrotrapezoid nucleus. Abnormally high levels of Pco2 cause an aversive interoceptive awareness in awake individuals and trigger arousal from sleep. These alerting responses presumably activate wake-promoting and/or stress-related pathways such as the orexinergic, noradrenergic, and serotonergic neurons. These neuronal groups, which may also be directly activated by brain acidification, have brainwide projections that contribute to the CO2-induced rise in breathing and SNA by facilitating neuronal activity at innumerable CNS locations. In the case of SNA, these sites include the nucleus of the solitary tract, the ventrolateral medulla, and the preganglionic neurons. en_US
dc.language.iso en en_US
dc.title Central CO2 chemoreception and integrated neural mechanisms of cardiovascular and respiratory control en_US
dc.type Article en_US
dc.description.version Published en_US
dc.author.school SOP en_US
dc.author.idnumber 201005298 en_US
dc.author.department N/A en_US
dc.description.embargo N/A en_US
dc.relation.journal Journal of Applied Physiology en_US
dc.journal.volume 108 en_US
dc.journal.issue 4 en_US
dc.article.pages 995-1002 en_US
dc.identifier.doi http://dx.doi.org/10.1152/japplphysiol.00712.2009 en_US
dc.identifier.ctation Guyenet, P. G., Stornetta, R. L., Abbott, S. B., Depuy, S. D., Fortuna, M. G., & Kanbar, R. (2010). Central CO2 chemoreception and integrated neural mechanisms of cardiovascular and respiratory control. Journal of applied physiology, 108(4), 995-1002. en_US
dc.author.email roy.kanbar@lau.edu.lb en_US
dc.identifier.tou http://libraries.lau.edu.lb/research/laur/terms-of-use/articles.php en_US
dc.identifier.url http://jap.physiology.org/content/108/4/995.short en_US
dc.orcid.id https://orcid.org/0000-0001-5450-6443 en_US

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