dc.contributorUniversidade Estadual Paulista (Unesp)
dc.date.accessioned2014-05-20T15:26:33Z
dc.date.accessioned2022-10-05T16:38:39Z
dc.date.available2014-05-20T15:26:33Z
dc.date.available2022-10-05T16:38:39Z
dc.date.created2014-05-20T15:26:33Z
dc.date.issued1996-02-01
dc.identifierBrazilian Journal of Medical and Biological Research. São Paulo: Associação Bras Divulg Cientifica, v. 29, n. 2, p. 245-247, 1996.
dc.identifier0100-879X
dc.identifierhttp://hdl.handle.net/11449/36705
dc.identifierWOS:A1996TV30300012
dc.identifier6551236936295697
dc.identifier1023597870118105
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/3908386
dc.description.abstractAngiotensin II (ANG II) administered centrally produces drinking by acting on subtype 1 ANG II (AT1) receptors, Carbachol, a cholinergic receptor agonist, also induces drinking behavior by a central action. In the present study we determined whether the response to carbachol also involves AT1 receptors. Male Holtzman rats (250-300 g) with stainless steel cannula implanted into the lateral ventricle (LV) were used. Water intake after injection of 0.15 M NaCl (1.0 mu l) into the LV was 0.2 +/- 0.01 ml/h (N = 8). The AT1 receptor antagonist DUP-753 (50 nmol/mu l) injected into the LV reduced water intake induced by ANG II (10 nmol/mu l) from 9.2 +/- 1.4 to 0.4 +/- 0.1 ml/h (N = 8), and water intake induced by carbachol (2 nmol/mu l) from 9.8 +/- 1.4 ml/h to 3.7 +/- 0.8 ml/h (N = 8), These results suggest that AT1 receptors play a role in the drinking behavior observed after central cholinergic stimulation in rats.
dc.languageeng
dc.publisherAssociação Brasileira de Divulgação Científica (ABRADIC)
dc.relationBrazilian Journal of Medical and Biological Research
dc.relation1.492
dc.rightsAcesso restrito
dc.sourceWeb of Science
dc.subjectwater intake
dc.subjectangiotensin 11
dc.subjectcarbachol
dc.subjectDUP-753
dc.subjectangiotensin receptor antagonist
dc.subjectAT1 receptor
dc.titleEffect of a non-peptide angiotensin receptor antagonist on water intake caused by centrally administered carbachol in the rat
dc.typeArtigo


Este ítem pertenece a la siguiente institución