A1 Noradrenergic Neurons Lesions Reduce Natriuresis and Hypertensive Responses to Hypernatremia in Rats

Show simple item record

dc.contributor.author Silva, Elaine Fernanda da
dc.contributor.author Freiria-Oliveira, Andre Henrique
dc.contributor.author Xavier Custodio, Carlos Henrique
dc.contributor.author Ghedini, Paulo Cesar
dc.contributor.author Mendes Bataus, Luiz Artur
dc.contributor.author Colombari, Eduardo
dc.contributor.author Castro, Carlos Henrique de
dc.contributor.author Colugnati, Diego Basile [UNIFESP]
dc.contributor.author Rosa, Daniel Alves
dc.contributor.author Cravo, Sergio Luiz [UNIFESP]
dc.contributor.author Pedrino, Gustavo Rodrigues
dc.date.accessioned 2016-01-24T14:34:24Z
dc.date.available 2016-01-24T14:34:24Z
dc.date.issued 2013-09-10
dc.identifier http://dx.doi.org/10.1371/journal.pone.0073187
dc.identifier.citation Plos One. San Francisco: Public Library Science, v. 8, n. 9, 11 p., 2013.
dc.identifier.issn 1932-6203
dc.identifier.uri http://repositorio.unifesp.br/handle/11600/36750
dc.description.abstract Noradrenergic neurons in the caudal ventrolateral medulla (CVLM; A1 group) contribute to cardiovascular regulation. the present study assessed whether specific lesions in the A1 group altered the cardiovascular responses that were evoked by hypertonic saline (HS) infusion in non-anesthetized rats. Male Wistar rats (280-340 g) received nanoinjections of antidopamine-beta-hydroxylase-saporin (A1 lesion, 0.105 ng.nL(-1)) or free saporin (sham, 0.021 ng.nL(-1)) into their CVLMs. Two weeks later, the rats were anesthetized (2% halothane in O-2) and their femoral artery and vein were catheterized and led to exit subcutaneously between the scapulae. On the following day, the animals were submitted to HS infusion (3 M NaCl, 1.8 ml . kg(-1), b.wt., for longer than 1 min). in the sham-group (n = 8), HS induced a sustained pressor response (Delta MAP: 35 +/- 3.6 and 11 +/- 1.8 mmHg, for 10 and 90 min after HS infusion, respectively; P<0.05 vs. baseline). Ten min after HS infusion, the pressor responses of the anti-D beta H-saporin-treated rats (n = 11) were significantly smaller(Delta MAP: 18 +/- 1.4 mmHg; P<0.05 vs. baseline and vs. sham group), and at 90 min, their blood pressures reached baseline values (2 +/- 1.6 mmHg). Compared to the sham group, the natriuresis that was induced by HS was reduced in the lesioned group 60 min after the challenge (19 +/- 65.5 mM vs. 262 +/- 7.6 mM, respectively; P<0.05). in addition, A1-lesioned rats excreted only 47% of their sodium 90 min after HS infusion, while sham animals excreted 80% of their sodium. Immunohistochemical analysis confirmed a substantial destruction of the A1 cell group in the CVLM of rats that had been nanoinjected withanti-D beta H-saporin. These results suggest that medullary noradrenergic A1 neurons are involved in the excitatory neural pathway that regulates hypertensive and natriuretic responses to acute changes in the composition of body fluid. en
dc.description.sponsorship Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
dc.description.sponsorship Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.description.sponsorship Fundacao de Amparo a Pesquisa do Estado de Goias (FAPEG)
dc.format.extent 11
dc.language.iso eng
dc.publisher Public Library Science
dc.relation.ispartof Plos One
dc.rights Acesso aberto
dc.title A1 Noradrenergic Neurons Lesions Reduce Natriuresis and Hypertensive Responses to Hypernatremia in Rats en
dc.type Artigo
dc.contributor.institution Universidade Federal de Goiás (UFG)
dc.contributor.institution São Paulo State Univ
dc.contributor.institution Universidade Federal de São Paulo (UNIFESP)
dc.description.affiliation Univ Fed Goias, Inst Biol Sci, Dept Physiol Sci, Goiania, Go, Brazil
dc.description.affiliation São Paulo State Univ, Sch Dent, Dept Physiol & Pathol, Araraquara, SP, Brazil
dc.description.affiliation Universidade Federal de São Paulo, Dept Physiol, São Paulo, Brazil
dc.description.affiliationUnifesp Universidade Federal de São Paulo, Dept Physiol, São Paulo, Brazil
dc.description.sponsorshipID CNPq: 477832/2010-5
dc.description.sponsorshipID CNPq: 483411/2012-4
dc.description.sponsorshipID Fundacao de Amparo a Pesquisa do Estado de Goias (FAPEG): 200910267000352
dc.identifier.file WOS000327538600019.pdf
dc.identifier.doi 10.1371/journal.pone.0073187
dc.description.source Web of Science
dc.identifier.wos WOS:000327538600019


Name: WOS000327538600019.pdf
Size: 1.527Mb
Format: PDF
Open file

This item appears in the following Collection(s)

Show simple item record




My Account