Effect of the gadolinium ion on body fluid regulation

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dc.contributor.authorPereira, Daniela de Toledo Borba [UNESP]
dc.contributor.authorNozaki, Priscila Nakada [UNESP]
dc.contributor.authorMenani, José Vanderlei [UNESP]
dc.contributor.authorColombari, Eduardo
dc.contributor.authorDe Luca, Laurival Antonio [UNESP]
dc.contributor.authorSchoorlemmer, Guus Hermanus Maria
dc.contributor.institutionUniversidade Estadual Paulista (Unesp)
dc.date.accessioned2015-12-07T15:29:43Z
dc.date.available2015-12-07T15:29:43Z
dc.date.issued2003
dc.description.abstractBoth osmoreception and baroreception are thought to involve ion channels that are sensitive to changes in membrane stretch. We investigated the effect of a blocker of stretch-activated ion channels, the Gd3+ ion, on osmoregulatory and cardiovascular responses in the intact rat. Intracerebroventricular injection of 50-100 nmol Gd3+ reduced thirst induced by various treatments. Similar doses also reduced intake of saline induced by various treatments. Intracerebroventricular injection of 100 nmol Gd3+ transiently increased arterial pressure and reduced the pressor response to intracerebroventricular angiotensin II (Ang II). Systemic administration of Gd3+ failed to alter thirst, except for a high dose (270 micromol/kg) that induced illness. This high dose failed to prevent urinary hypertonicity and excretion of a load of hypertonic NaCl. Intravenous infusion of 270 micromol/kg of Gd3+ reduced blood pressure and pressure responses to intravenous phenylephrine, but did not reduce the baroreceptor reflex control of heart rate. We conclude that the effects of Gd3+ on thirst and on the cardiovascular system are probably not due to a direct effect of the drug on stretch-sensitive ion channels. Instead, many of the effects of Gd3+ were compatible with blockade of voltage-gated Ca2+ channels.en
dc.description.affiliationDepartment of Physiology and Pathology, Paulista State University (UNESP), Brazil
dc.description.affiliationUnespDepartment of Physiology and Pathology, Paulista State University (UNESP), Brazil
dc.description.sponsorshipConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
dc.description.sponsorshipFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
dc.format.extent275-283
dc.identifierhttp://dx.doi.org/10.1016/j.pbb.2003.08.001
dc.identifier.citationPharmacology, Biochemistry, And Behavior, v. 76, n. 2, p. 275-283, 2003.
dc.identifier.doi10.1016/j.pbb.2003.08.001
dc.identifier.issn0091-3057
dc.identifier.lattes1023597870118105
dc.identifier.lattes4544450092427426
dc.identifier.pubmed14592679
dc.identifier.urihttp://hdl.handle.net/11449/130845
dc.language.isoeng
dc.publisherElsevier
dc.relation.ispartofPharmacology, Biochemistry, And Behavior
dc.relation.ispartofjcr2.538
dc.relation.ispartofsjr1,150
dc.rights.accessRightsAcesso restrito
dc.sourcePubMed
dc.subjectStretch-sensitive ion channelsen
dc.subjectGadoliniumen
dc.subjectThirsten
dc.subjectSodium intakeen
dc.subjectOsmoreceptorsen
dc.subjectBaroreceptorsen
dc.titleEffect of the gadolinium ion on body fluid regulationen
dc.typeArtigo
dcterms.rightsHolderElsevier
unesp.author.lattes1023597870118105
unesp.author.lattes4544450092427426[4]
unesp.author.orcid0000-0002-1395-4036[4]
unesp.author.orcid0000-0003-1167-4441[3]
unesp.campusUniversidade Estadual Paulista (Unesp), Faculdade de Odontologia, Araraquarapt

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