Efferent pathways in sodium overload-induced renal vasodilation in rats

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dc.creatorAmaral, Nathalia Oda
dc.creatorOliveira, Thiago S. de
dc.creatorNaves, Lara Marques
dc.creatorFilgueira, Fernando P.
dc.creatorFerreira-Neto, Marcos Luiz
dc.creatorSchoorlemmer, Gerhardus Hermanus Maria
dc.creatorCastro, Carlos Henrique de
dc.creatorOliveira, Andre Henrique Freiria
dc.creatorCustódio, Carlos Henrique Xavier
dc.creatorColugnati, Diego Basile
dc.creatorRosa, Daniel Alves
dc.creatorBlanch, Graziela Torres
dc.creatorBorges, Clayton Luiz
dc.creatorSoares, Célia Maria de Almeida
dc.creatorReis, Angela Adamski da Silva
dc.creatorCravo, Sergio Luiz Domingues
dc.creatorPedrino, Gustavo Rodrigues
dc.date.accessioned2018-07-10T11:41:51Z
dc.date.available2018-07-10T11:41:51Z
dc.date.issued2014-10
dc.description.abstractHypernatremia stimulates the secretion of oxytocin (OT), but the physiological role of OT remains unclear. The present study sought to determine the involvement of OT and renal nerves in the renal responses to an intravenous infusion of hypertonic saline. Male Wistar rats (280–350 g) were anesthetized with sodium thiopental (40 mg. kg 21 , i.v.). A bladder cannula was implanted for collection of urine. Animals were also instrumented for measurement of mean arterial pressure (MAP) and renal blood flow (RBF). Renal vascular conductance (RVC) was calculated as the ratio of RBF by MAP. In anesthetized rats (n = 6), OT infusion (0.03 m g N kg 21 , i.v.) induced renal vasodilation. Consistent with this result, ex vivo experiments demonstrated that OT caused renal artery relaxation. Blockade of OT receptors (OXTR) reduced these responses to OT, indicating a direct effect of this peptide on OXTR on this artery. Hypertonic saline (3 M NaCl, 1.8 ml N kg 21 b.wt., i.v.) was infused over 60 s. In sham rats (n = 6), hypertonic saline induced renal vasodilation. The OXTR antagonist (AT; atosiban, 40 m g N kg 21 N h 21 , i.v.; n = 7) and renal denervation (RX) reduced the renal vasodilation induced by hypernatremia. The combination of atosiban and renal denervation (RX+AT; n = 7) completely abolished the renal vasodilation induced by sodium overload. Intact rats excreted 51% of the injected sodium within 90 min. Natriuresis was slightly blunted by atosiban and renal denervation (42% and 39% of load, respectively), whereas atosiban with renal denervation reduced sodium excretion to 16% of the load. These results suggest that OT and renal nerves are involved in renal vasodilation and natriuresis induced by acute plasma hypernatremia.pt_BR
dc.identifier.citationAMARAL, Nathalia O.; OLIVEIRA, Thiago S. de; NAVES, Lara M.; FILGUEIRA, Fernando P.; FERREIRA-NETO, Marcos L.; SCHOORLEMMER, Gerard H. M.; CASTRO, Carlos H. de; FREIRIA-OLIVEIRA, André H.; XAVIER, Carlos H.; COLUGNATI, Diego B.; ROSA, Daniel A.; BLANCH, Graziela T.; BORGES, Clayton L. ; SOARES, Célia M. A.; REIS, Angela A. S.; CRAVO, Sergio L.; PEDRINO, Gustavo R. Efferent pathways in sodium overload-induced renal vasodilation in rats. Plos One, San Franisco, v. 9, n. 10, e109620, Oct. 2014.pt_BR
dc.identifier.doi10.1371/journal.pone.0109620
dc.identifier.issne- 1932-6203
dc.identifier.urihttp://repositorio.bc.ufg.br/handle/ri/15372
dc.language.isoengpt_BR
dc.publisher.countryEstados unidospt_BR
dc.publisher.departmentInstituto de Ciências Biológicas - ICB (RG)pt_BR
dc.rightsAcesso Abertopt_BR
dc.titleEfferent pathways in sodium overload-induced renal vasodilation in ratspt_BR
dc.typeArtigopt_BR

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