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Central moxonidine on salivary gland blood flow and cardiovascular responses to pilocarpine

dc.contributor.authorMoreira, T. S.
dc.contributor.authorTakakura, ACT
dc.contributor.authorColombari, Eduardo [UNESP]
dc.contributor.authorDe Luca, L. A.
dc.contributor.authorRenzi, Antonio [UNESP]
dc.contributor.authorMenani, José Vanderlei [UNESP]
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.contributor.institutionUniversidade Federal de São Paulo (UNIFESP)
dc.date.accessioned2014-05-20T13:45:49Z
dc.date.available2014-05-20T13:45:49Z
dc.date.issued2003-10-17
dc.description.abstractPeripheral treatment with the cholinergic agonist pilocarpine induces intense salivation that is inhibited by central injections of the alpha(2)-adrenergic/imidazoline receptor agonist moxonidine. Salivary gland blood flow controlled by sympathetic and parasympathetic systems may affect salivation. We investigated the changes in mean arterial pressure (MAP) and in the vascular resistance in the submandibular/sublingual gland (SSG) artery, superior mesenteric (SM) artery and low abdominal aorta (hindlimb) in rats treated with intraperitoneal (i.p.) pilocarpine alone or combined with intracerebroventricular (i.c.v.) moxonidine. Male Holtzman rats with stainless steel cannula. implanted into lateral ventricle (LV) and anesthetized with urethane were used. Pilocarpine (4 mumol/kg of body weight) i.p. reduced SSG vascular resistance (-50 +/- 13% vs. vehicle: 5 +/- 3%). Pilocarpine i.p. also increased mesenteric vascular resistance (15 +/- 5% vs. vehicle: 2 +/- 3%) and MAP (16 +/- 3 mmHg, vs. vehicle: 2 +/- 3 mmHg). Moxonidine (20 nmol) i.c.v. increased SSG vascular resistance (88 +/- 12% vs. vehicle: 7 +/- 4%). When injected 15 min following i.c.v. moxonidine, pilocarpine i.p. produced no change on SSG vascular resistance. Pilocarpine-induced pressor responses and increase in mesenteric vascular resistance were not modified by i.c.v. moxonidine. The treatments produced no change in heart rate (HR) and hindlimb vascular resistance. The results show that (1) i.p. pilocarpine increases mesenteric vascular resistance and MAP and reduces salivary gland vascular resistance and (2) central moxonidine increases salivary gland vascular resistance and impairs pilocarpine-induced salivary gland vasodilatation. Therefore, the increase in salivary gland vascular resistance may play a role in the anti-salivatory response to central moxonidine. (C) 2003 Elsevier B.V. All rights reserved.en
dc.description.affiliationUniv Estadual Paulista, UNESP, Fac Odontol, Dept Fisiol & Patol, BR-14801903 Araraquara, SP, Brazil
dc.description.affiliationUniv Fed São Paulo, Escola Paulista Med, Dept Fisiol, BR-04023060 São Paulo, SP, Brazil
dc.description.affiliationUnespUniv Estadual Paulista, UNESP, Fac Odontol, Dept Fisiol & Patol, BR-14801903 Araraquara, SP, Brazil
dc.format.extent155-163
dc.identifierhttp://dx.doi.org/10.1016/S0006-8993(03)03322-5
dc.identifier.citationBrain Research. Amsterdam: Elsevier B.V., v. 987, n. 2, p. 155-163, 2003.
dc.identifier.doi10.1016/S0006-8993(03)03322-5
dc.identifier.issn0006-8993
dc.identifier.lattes4544450092427426
dc.identifier.lattes6551236936295697
dc.identifier.lattes1023597870118105
dc.identifier.urihttp://hdl.handle.net/11449/16161
dc.identifier.wosWOS:000185945900003
dc.language.isoeng
dc.publisherElsevier B.V.
dc.relation.ispartofBrain Research
dc.relation.ispartofjcr3.125
dc.relation.ispartofsjr1,404
dc.rights.accessRightsAcesso restritopt
dc.sourceWeb of Science
dc.subjectalpha(2)-adrenergic and imidazoline receptorpt
dc.subjectcholinergic agonistpt
dc.subjectparasympatheticpt
dc.subjectblood flow and vascular resistancept
dc.subjectsalivary glandpt
dc.titleCentral moxonidine on salivary gland blood flow and cardiovascular responses to pilocarpineen
dc.typeArtigopt
dcterms.licensehttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dcterms.rightsHolderElsevier B.V.
dspace.entity.typePublication
relation.isDepartmentOfPublicationb3ba3d9c-022e-4521-8805-0bcceea7372e
relation.isDepartmentOfPublication.latestForDiscoveryb3ba3d9c-022e-4521-8805-0bcceea7372e
relation.isOrgUnitOfPublicationca4c0298-cd82-48ee-a9c8-c97704bac2b0
relation.isOrgUnitOfPublication.latestForDiscoveryca4c0298-cd82-48ee-a9c8-c97704bac2b0
unesp.author.lattes4544450092427426[3]
unesp.author.lattes6551236936295697
unesp.author.lattes1023597870118105
unesp.author.orcid0000-0002-1395-4036[3]
unesp.author.orcid0000-0003-1167-4441[6]
unesp.campusUniversidade Estadual Paulista (UNESP), Faculdade de Odontologia, Araraquarapt
unesp.departmentFisiologia e Patologia - FOARpt

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