Please use this identifier to cite or link to this item: https://repositorio.unifesp.br/handle/11600/38321
Title: Efferent Pathways in Sodium Overload-Induced Renal Vasodilation in Rats
Authors: Amaral, Nathalia O.
Oliveira, Thiago S. de
Naves, Lara M.
Filgueira, Fernando P.
Ferreira-Neto, Marcos L.
Schoorlemmer, Gerhardus Hermanus Maria [UNIFESP]
Castro, Carlos H. de
Freiria-Oliveira, Andre H.
Xavier, Carlos H.
Colugnati, Diego Basile [UNIFESP]
Rosa, Daniel A.
Blanch, Graziela T.
Borges, Clayton L.
Soares, Celia M. A.
Reis, Angela A. S.
Cravo, Sergio Luiz [UNIFESP]
Pedrino, Gustavo R.
Universidade Federal de Goiás (UFG)
Universidade Federal de Uberlândia (UFU)
Universidade Federal de São Paulo (UNIFESP)
Issue Date: 3-Oct-2014
Publisher: Public Library Science
Citation: Plos One. San Francisco: Public Library Science, v. 9, n. 10, 10 p., 2014.
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(-1), 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 mu g . kg(-1), 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 . kg(-1) 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 mu g . kg(-1) . h(-1), 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.
URI: http://repositorio.unifesp.br/handle/11600/38321
ISSN: 1932-6203
Other Identifiers: http://dx.doi.org/10.1371/journal.pone.0109620
Appears in Collections:Em verificação - Geral

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