dc.creatorGuadagnini, D
dc.creatorGontijo, JAR
dc.date2006
dc.dateSEP 20
dc.date2014-11-14T20:14:57Z
dc.date2015-11-26T16:08:10Z
dc.date2014-11-14T20:14:57Z
dc.date2015-11-26T16:08:10Z
dc.date.accessioned2018-03-28T22:56:43Z
dc.date.available2018-03-28T22:56:43Z
dc.identifierLife Sciences. Pergamon-elsevier Science Ltd, v. 79, n. 17, n. 1666, n. 1673, 2006.
dc.identifier0024-3205
dc.identifierWOS:000241024300011
dc.identifier10.1016/j.lfs.2006.06.005
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/77232
dc.identifierhttp://www.repositorio.unicamp.br/handle/REPOSIP/77232
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/77232
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1266289
dc.descriptionThe mechanism by which blood pressure rises in the SHR strain remains to be elucidated. Also, there is a surprising lack of experimental data on the natriuretic mechanisms induced by intracerebroventricular (ICV) injection of hyperosmotic saline (HoS) in SHR. In normotensive animals ICV injection of HoS causes coordinated responses including natriuresis and inhibition of renal sympathetic nerve activity. In the present study, we hypothesized that presumable blunting of the sympathoinhibitory response to centrally injected HoS may contribute to a lack of suppression of efferent renal nerve outflow in SHR. To test this hypothesis, the present study evaluates the influence of renal denervation after central HoS injection at increasing concentration on urinary sodium handling in SHR compared with age-matched normotensive WKy rats. The study confirmed previous data showing pronounced natriuretic response to centrally HoS stimuli but also demonstrated that the creatinine clearance (C-Cr) and fractional sodium excretion responses diminished as graded NaCl concentrations were increased in WKy rats but not in SHR. In SHR, increased FENa obtained by central administration of 0.90 M NaCl was produced by increases in proximal (FEPNa) and post-proximal fractional urinary sodium rejection without changes in C-Cr, indicating a direct tubular effect. Renal denervation caused significant antinatriuresis by decreased C-Cr and increased FEPNa reabsorption in WKy but not in SHR. This study suggests that natriuresis observed only after higher centrally HoS stimuli with a rightward shift of dose-response curve provides evidence of a down-regulation of target organ responsiveness of periventricular areas of genetic hypertensive rats. (c) 2006 Elsevier Inc. All rights reserved.
dc.description79
dc.description17
dc.description1666
dc.description1673
dc.languageen
dc.publisherPergamon-elsevier Science Ltd
dc.publisherOxford
dc.publisherInglaterra
dc.relationLife Sciences
dc.relationLife Sci.
dc.rightsfechado
dc.rightshttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dc.sourceWeb of Science
dc.subjectarterial hypertension
dc.subjecthypertonic saline
dc.subjectSHR
dc.subjectkidney denervation
dc.subjectnatriuresis
dc.subjectlithium clearance
dc.subjectNitric-oxide Synthase
dc.subjectBlood-pressure
dc.subjectArterial-pressure
dc.subjectNatriuresis
dc.subjectSalt
dc.subjectKidney
dc.subjectInhibition
dc.subjectMetabolism
dc.subjectMechanisms
dc.subjectReactivity
dc.titleAltered renal sodium handling in spontaneously hypertensive rats (SHR) after hypertonic saline intracerebroventricular injection: Role of renal nerves
dc.typeArtículos de revistas


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