dc.creatorMichelotto, JB
dc.creatorCarvalheira, JBC
dc.creatorSaad, MJA
dc.creatorGontijo, JAR
dc.date2002
dc.date42064
dc.date2014-11-17T21:50:06Z
dc.date2015-11-26T17:42:38Z
dc.date2014-11-17T21:50:06Z
dc.date2015-11-26T17:42:38Z
dc.date.accessioned2018-03-29T00:24:34Z
dc.date.available2018-03-29T00:24:34Z
dc.identifierBrain Research Bulletin. Pergamon-elsevier Science Ltd, v. 57, n. 5, n. 613, n. 618, 2002.
dc.identifier0361-9230
dc.identifierWOS:000174792200007
dc.identifier10.1016/S0361-9230(01)00754-7
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/64985
dc.identifierhttp://www.repositorio.unicamp.br/handle/REPOSIP/64985
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/64985
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1287355
dc.descriptionThe role of the central nervous system (CNS) in the control of hydrosaline homeostasis has been strikingly demonstrated by several studies. Growing evidence suggests that insulin may exert an influence in the modulation of many brain functions. However, there are no available data examining the CNS effect of insulin injection on renal sodium handling. Also, to examine the influence of renal nerve activity during i.c.v. administration of insulin, unanesthetized, unrestrained rats were randomly assigned to one of nine separated groups: (a) sham-operated i.c.v. 0.15 M NaCl-injected (Co, pooled data, n = 37) and sham-operated i.c.v. 0.42 ng.mul(-1) (n = 12), 4.2 ng.mul(-1) (n = 10) and 42.0 ng.mul(-1) (n = 11) insulin-injected rats (In);, (b) renal-denervated i.c.v. 0.15 M NaCl (Co-Dx, n = 5), and insulin-injected rats (In-Dx, n = 5); and (c) subcutaneously insulin-injected rats (SC, n = 5). We showed that centrally administered insulin produced dose-related increased urinary output of sodium [Co: 855 +/- 85 Delta% min, 0.42 ng.mul(-1)In 1189 +/- 308 Delta% min, 4.2 ng.mul(-1)In: 1461 +/- 594 Delta% min (p = 0.048), and 42.0 ng.mul(-1)In: 2055 +/- 411 Delta% min (p = 0.0001)], and dose-independently increased potassium excretion [Co: 460 +/- 28 Delta% min, 0.42 ng.mul(-1)In: 649 +/- 100 Delta% min (p = 0.016), 4.2 ng.mul(-1)In: 671 +/- 175 +/- min (p = 0.003), and 42.0 ng.mul(-1)In: 669 +/- 70 Delta% min (p = 0.002)] compared to control. The urinary sodium excretion response to i.c.v. 42 ng.mul(-1) insulin injections were abolished by bilateral renal denervation. In addition, we showed that insulin-induced natriuresis occurred by increasing postproximal tubule sodium rejection (FEPPNa), and changed glomerular filtration rate (C-Cr) at 42.0 ng.mul(-1) (p = 0.023) i.c.v. insulin microinjection but not at smaller insulin dose. The current data suggests that a blunted efferent insulin-sensitive nerve activity from periventricular region may contribute to the inability of renal tubules to handle the hydroelectrolyte balance. (C) 2002 Elsevier Science Inc.
dc.description57
dc.description5
dc.description613
dc.description618
dc.languageen
dc.publisherPergamon-elsevier Science Ltd
dc.publisherOxford
dc.publisherInglaterra
dc.relationBrain Research Bulletin
dc.relationBrain Res. Bull.
dc.rightsfechado
dc.rightshttp://www.elsevier.com/about/open-access/open-access-policies/article-posting-policy
dc.sourceWeb of Science
dc.subjectcentral nervous system
dc.subjectintracerebroventricular
dc.subjectinsulin
dc.subjectnatriuresis
dc.subjectrenal denervation
dc.subjectlithium clearance
dc.subjectObese Zucker Rats
dc.subjectHyperinsulinemia
dc.subjectHypothalamus
dc.subjectMetabolism
dc.subjectGlucose
dc.subjectBinding
dc.subjectNerves
dc.subjectBrain
dc.titleEffects of intracerebroventricular insulin microinjection on renal sodium handling in kidney-denervated rats
dc.typeArtículos de revistas


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