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dc.contributor.authorAbdala, Ana Paula L.
dc.contributor.authorSchoorlemmer, Guus H. M.
dc.contributor.authorColombari, Eduardo [UNESP]
dc.date.accessioned2014-05-20T13:45:48Z
dc.date.available2014-05-20T13:45:48Z
dc.date.issued2006-11-13
dc.identifierhttp://dx.doi.org/10.1016/j.brainres.2006.08.059
dc.identifier.citationBrain Research. Amsterdam: Elsevier B.V., v. 1119, p. 165-173, 2006.
dc.identifier.issn0006-8993
dc.identifier.urihttp://hdl.handle.net/11449/16145
dc.description.abstractThe nucleus of the solitary tract (NTS) receives primary afferents involved in cardiovascular regulation. We investigated the role of NK1-receptor bearing neurons in the NTS on cardiovascular reflexes in awake rats fitted with chronic venous and arterial cannulae. These neurons were lesioned selectively with saporin conjugated with substance P (SP-SAP, 2 mu M, bilateral injections of 20 nL in the subpostremal NTS, or 200 nL in both the subpostremal and the commissural NTS). Before, and 7 and 14 days after injection of SP-SAP, we measured changes in blood pressure and heart rate induced by i.v. injection of phenylephrine and nitroprusside (baroreceptor reflex), cyanide (arterial chemoreceptor reflex), and phenylbiguanide (Bezold-Jarisch reflex). The smaller injections with SP-SAP completely abolished NK1 receptor staining in the subpostremal NTS. The larger injections abolished NK1 receptor immunoreactivity in an area that extended from the commissural NTS to the rostral end of the subpostremal NTS. The lesions seemed to affect only a limited number of neurons, since neutral red stained sections did not show any obvious reduction in cell number. The smaller lesions reduced the gain of baroreflex bradycardia and the hypotension induced by phenylbiguanide. The larger lesions completely abolished the response to phenylbiguanide, blocked the baroreflex bradycardia induced by phenylephrine, severely blunted the baroreflex tachycardia, and blocked the bradycardia and reduced the hypertension induced by cyanide. Thus, these responses depend critically on NK1-receptor bearing neurons in the NTS. (c) 2006 Elsevier B.V. All rights reserved.en
dc.format.extent165-173
dc.language.isoeng
dc.publisherElsevier B.V.
dc.relation.ispartofBrain Research
dc.sourceWeb of Science
dc.subjecttachykininpt
dc.subjectbaroreflexpt
dc.subjectchemoreflexpt
dc.subjectBezold-Jarisch reflexpt
dc.subjectnucleus of the solitary tractpt
dc.subjectsubstance Ppt
dc.titleAblation of NK1 receptor bearing neurons in the nucleus of the solitary tract blunts cardiovascular reflexes in awake ratsen
dc.typeArtigo
dcterms.licensehttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dcterms.rightsHolderElsevier B.V.
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.description.affiliationUniv Fed São Paulo, Dept Fisiol, EPM, BR-04023062 São Paulo, Brazil
dc.description.affiliationUniv Estadual Paulista, Fac Odontol, Dept Physiol, BR-14801903 Araraquara, SP, Brazil
dc.description.affiliationUnespUniv Estadual Paulista, Fac Odontol, Dept Physiol, BR-14801903 Araraquara, SP, Brazil
dc.identifier.doi10.1016/j.brainres.2006.08.059
dc.identifier.wosWOS:000242309600016
dc.rights.accessRightsAcesso restrito
unesp.campusUniversidade Estadual Paulista (Unesp), Faculdade de Odontologia, Araraquarapt
dc.identifier.lattes4544450092427426
unesp.author.lattes4544450092427426[3]
unesp.author.orcid0000-0002-1395-4036[3]
dc.relation.ispartofjcr3.125
dc.relation.ispartofsjr1,404
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