Use este identificador para citar ou linkar para este item: http://repositorio.bc.ufg.br/handle/ri/15372
Tipo do documento: Artigo
Título: Efferent pathways in sodium overload-induced renal vasodilation in rats
Autor: Amaral, Nathalia Oda
Oliveira, Thiago S. de
Naves, Lara Marques
Filgueira, Fernando P.
Ferreira-Neto, Marcos Luiz
Schoorlemmer, Gerhardus Hermanus Maria
Castro, Carlos Henrique de
Oliveira, Andre Henrique Freiria
Custódio, Carlos Henrique Xavier
Colugnati, Diego Basile
Rosa, Daniel Alves
Blanch, Graziela Torres
Borges, Clayton Luiz
Soares, Célia Maria de Almeida
Reis, Angela Adamski da Silva
Cravo, Sergio Luiz Domingues
Pedrino, Gustavo Rodrigues
Abstract: Hypernatremia 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.
País: Estados unidos
Unidade acadêmica: Instituto de Ciências Biológicas - ICB (RG)
Citação: AMARAL, 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.
Tipo de acesso: Acesso Aberto
Identificador do documento: 10.1371/journal.pone.0109620
Identificador do documento: 10.1371/journal.pone.0109620
URI: http://repositorio.bc.ufg.br/handle/ri/15372
Data de publicação: Out-2014
Aparece nas coleções:IPTSP - Artigos publicados em periódicos

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