Central moxonidine on salivary gland blood flow and cardiovascular responses to pilocarpine
dc.contributor.author | Moreira, T. S. | |
dc.contributor.author | Takakura, ACT | |
dc.contributor.author | Colombari, Eduardo [UNESP] | |
dc.contributor.author | De Luca, L. A. | |
dc.contributor.author | Renzi, Antonio [UNESP] | |
dc.contributor.author | Menani, José Vanderlei [UNESP] | |
dc.contributor.institution | Universidade Estadual Paulista (Unesp) | |
dc.contributor.institution | Universidade Federal de São Paulo (UNIFESP) | |
dc.date.accessioned | 2014-05-20T13:45:49Z | |
dc.date.available | 2014-05-20T13:45:49Z | |
dc.date.issued | 2003-10-17 | |
dc.description.abstract | Peripheral 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.affiliation | Univ Estadual Paulista, UNESP, Fac Odontol, Dept Fisiol & Patol, BR-14801903 Araraquara, SP, Brazil | |
dc.description.affiliation | Univ Fed São Paulo, Escola Paulista Med, Dept Fisiol, BR-04023060 São Paulo, SP, Brazil | |
dc.description.affiliationUnesp | Univ Estadual Paulista, UNESP, Fac Odontol, Dept Fisiol & Patol, BR-14801903 Araraquara, SP, Brazil | |
dc.format.extent | 155-163 | |
dc.identifier | http://dx.doi.org/10.1016/S0006-8993(03)03322-5 | |
dc.identifier.citation | Brain Research. Amsterdam: Elsevier B.V., v. 987, n. 2, p. 155-163, 2003. | |
dc.identifier.doi | 10.1016/S0006-8993(03)03322-5 | |
dc.identifier.issn | 0006-8993 | |
dc.identifier.lattes | 4544450092427426 | |
dc.identifier.lattes | 6551236936295697 | |
dc.identifier.lattes | 1023597870118105 | |
dc.identifier.uri | http://hdl.handle.net/11449/16161 | |
dc.identifier.wos | WOS:000185945900003 | |
dc.language.iso | eng | |
dc.publisher | Elsevier B.V. | |
dc.relation.ispartof | Brain Research | |
dc.relation.ispartofjcr | 3.125 | |
dc.relation.ispartofsjr | 1,404 | |
dc.rights.accessRights | Acesso restrito | pt |
dc.source | Web of Science | |
dc.subject | alpha(2)-adrenergic and imidazoline receptor | pt |
dc.subject | cholinergic agonist | pt |
dc.subject | parasympathetic | pt |
dc.subject | blood flow and vascular resistance | pt |
dc.subject | salivary gland | pt |
dc.title | Central moxonidine on salivary gland blood flow and cardiovascular responses to pilocarpine | en |
dc.type | Artigo | pt |
dcterms.license | http://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy | |
dcterms.rightsHolder | Elsevier B.V. | |
dspace.entity.type | Publication | |
relation.isDepartmentOfPublication | b3ba3d9c-022e-4521-8805-0bcceea7372e | |
relation.isDepartmentOfPublication.latestForDiscovery | b3ba3d9c-022e-4521-8805-0bcceea7372e | |
relation.isOrgUnitOfPublication | ca4c0298-cd82-48ee-a9c8-c97704bac2b0 | |
relation.isOrgUnitOfPublication.latestForDiscovery | ca4c0298-cd82-48ee-a9c8-c97704bac2b0 | |
unesp.author.lattes | 4544450092427426[3] | |
unesp.author.lattes | 6551236936295697 | |
unesp.author.lattes | 1023597870118105 | |
unesp.author.orcid | 0000-0002-1395-4036[3] | |
unesp.author.orcid | 0000-0003-1167-4441[6] | |
unesp.campus | Universidade Estadual Paulista (UNESP), Faculdade de Odontologia, Araraquara | pt |
unesp.department | Fisiologia e Patologia - FOAR | pt |
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