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Carotid body function and ventilatory responses in intermittent hypoxia. evidence for anomalous brainstem integration of arterial chemoreceptor input

2011-08-01Artigo científico Acesso aberto
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dc.contributor.authorGonzalez-Martín, M. C.
dc.contributor.authorVega-Agapito, M. V.
dc.contributor.authorConde, S. V.
dc.contributor.authorV Conde, Silvia
dc.contributor.authorCastañeda, J.
dc.contributor.authorBustamante, R.
dc.contributor.authorOlea, E.
dc.contributor.authorPerez-Vizcaino, F.
dc.contributor.authorGonzalez, C.
dc.contributor.authorObeso, A.
dc.contributor.institutionNOVA Medical School|Faculdade de Ciências Médicas (NMS|FCM)
dc.contributor.institutionCentro de Estudos de Doenças Crónicas (CEDOC)
dc.contributor.pblJohn Wiley & Sons, Ltd.
dc.date.accessioned2023-12-28T22:11:16Z
dc.date.available2023-12-28T22:11:16Z
dc.date.issued2011-08-01
dc.description.abstractObstructive sleep apnea is a frequent medical condition consisting in repetitive sleep-related episodes of upper airways obstruction and concurrent events of arterial blood hypoxia. There is a frequent association of cardiovascular diseases and other pathologies to this condition conforming the obstructive sleep apnea syndrome (OSAS). Laboratory models of OSAS consist in animals exposed to repetitive episodes of intermittent hypoxia (IH) which also develop cardiovascular pathologies, mostly hypertension. The overall OSAS pathophysiology appears to be linked to the repetitive hypoxia, which would cause a sensitization of carotid body (CB) chemoreflex and chemoreflex-driven hyperreactivity of the sympathetic nervous system. However, this proposal is uncertain because hyperventilation, reflecting the CB sensitization, and increased plasma CA levels, reflecting sympathetic hyperreactivity, are not constant findings in patients with OSAS and IH animals. Aiming to solve these uncertainties we have studied the entire CB chemoreflex arch in a rat model of IH, including activity of chemoreceptor cells and CB generated afferent activity to brainstem. The efferent activity was measured as ventilation in normoxia, hypoxia, and hypercapnia. Norepinephrine turnover in renal artery sympathetic endings was also assessed. Findings indicate a sensitization of the CB function to hypoxia evidenced by exaggerated chemoreceptor cell and CB afferent activity. Yet, IH rats exhibited marked hypoventilation in all studied conditions and increased turnover of norepinephrine in sympathetic endings. We conclude that IH produces a bias in the integration of the input arising from the CB with a diminished drive of ventilation and an exaggerated activation of brainstem sympathetic neurons.en
dc.description.versionpublishersversion
dc.description.versionpublished
dc.format.extent9
dc.format.extent331376
dc.identifier.doi10.1002/jcp.22528
dc.identifier.issn0021-9541
dc.identifier.otherPURE: 6180648
dc.identifier.otherPURE UUID: c80659aa-c29f-4a77-90b6-b1821f01a235
dc.identifier.otherScopus: 79955105687
dc.identifier.otherPubMed: 21520047
dc.identifier.otherWOS: 000290520900001
dc.identifier.otherORCID: /0000-0002-5920-5700/work/111135940
dc.identifier.urihttp://hdl.handle.net/10362/161713
dc.identifier.urlhttps://www.scopus.com/pages/publications/79955105687
dc.language.isoeng
dc.peerreviewedyes
dc.subjectPhysiology
dc.subjectClinical Biochemistry
dc.subjectCell Biology
dc.subjectSDG 3 - Good Health and Well-being
dc.titleCarotid body function and ventilatory responses in intermittent hypoxia. evidence for anomalous brainstem integration of arterial chemoreceptor inputen
dc.typejournal article
degois.publication.firstPage1961
degois.publication.issue8
degois.publication.lastPage1969
degois.publication.titleJournal Of Cellular Physiology
degois.publication.volume226
dspace.entity.typePublication
person.familyNameVilares Conde
person.givenNameSilvia
person.identifier154176
person.identifier.ciencia-id561E-CF29-600A
person.identifier.orcid0000-0002-5920-5700
person.identifier.scopus-author-id7004283202
rcaap.rightsopenAccess
relation.isAuthorOfPublication898e99d8-61a5-44bc-878a-5e1ac44ca37c
relation.isAuthorOfPublication.latestForDiscovery898e99d8-61a5-44bc-878a-5e1ac44ca37c

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