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dc.contributor.authorCayzac, A.
dc.contributor.authorRocher Martín, María Asunción 
dc.contributor.authorObeso Cáceres, Ana María de la Luz 
dc.contributor.authorGonzález, Constancio
dc.contributor.authorRicardi, D.
dc.contributor.authorKemp, P. K.
dc.date.accessioned2014-11-12T12:46:00Z
dc.date.available2014-11-12T12:46:00Z
dc.date.issued2011
dc.identifier.citationRespiratory Physiology & Neurobiology 175 (2011) 80–89es
dc.identifier.issn1569-9048es
dc.identifier.urihttp://uvadoc.uva.es/handle/10324/7091
dc.descriptionInnovación Educativaes
dc.description.abstractAn increase in intracellular Ca2+ is crucial to O2 sensing by the carotid body. Polyamines have been reported to modulate both the extracellular Ca2+-sensing receptor (CaR) and voltage-gated Ca2+ channels in a number of cell types. Using RT-PCR and immunohistochemistry, the predominant voltage-gated Ca2+ channels expressed in the adult rat carotid body were L (CaV1.2) and N (CaV2.2)-type. CaR mRNA could not be amplified from carotid bodies, but the protein was expressed in the nerve endings. Spermine inhibited the hypoxia-evoked catecholamine release from isolated carotid bodies and attenuated the depolarization- and hypoxia-evoked Ca2+ influx into isolated glomus cells. In agreement with data from carotid body, recombinant CaV1.2 was also inhibited by spermine. In contrast, the positive allosteric modulator of CaR, R-568, was without effect on hypoxia-induced catecholamine release from carotid bodies and depolarization-evoked Ca2+ influx into glomus cells. These data show that spermine exerts a negative influence on carotid body O2 sensing by inhibiting L-type Ca2+ channels.es
dc.format.mimetypeapplication/pdfes
dc.language.isoenges
dc.publisherElsevieres
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/
dc.subjectRespiración celulares
dc.titleSpermine attenuates carotid body glomus cell oxygen sensing by inhibitinges
dc.typeinfo:eu-repo/semantics/articlees
dc.identifier.doi10.1016/j.resp.2010.09.009es
dc.identifier.publicationfirstpage80es
dc.identifier.publicationlastpage89es
dc.identifier.publicationtitleRespiratory Physiology & Neurobiologyes
dc.identifier.publicationvolume175es
dc.peerreviewedes
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 International


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