Efferent Pathways in Sodium Overload-Induced Renal Vasodilation in Rats

Efferent Pathways in Sodium Overload-Induced Renal Vasodilation in Rats

Author Amaral, Nathalia O. Google Scholar
Oliveira, Thiago S. de Google Scholar
Naves, Lara M. Google Scholar
Filgueira, Fernando P. Google Scholar
Ferreira-Neto, Marcos L. Google Scholar
Schoorlemmer, Gerhardus Hermanus Maria Autor UNIFESP Google Scholar
Castro, Carlos H. de Google Scholar
Freiria-Oliveira, Andre H. Google Scholar
Xavier, Carlos H. Google Scholar
Colugnati, Diego Basile Autor UNIFESP Google Scholar
Rosa, Daniel A. Google Scholar
Blanch, Graziela T. Google Scholar
Borges, Clayton L. Google Scholar
Soares, Celia M. A. Google Scholar
Reis, Angela A. S. Google Scholar
Cravo, Sergio Luiz Autor UNIFESP Google Scholar
Pedrino, Gustavo R. Google Scholar
Institution Universidade Federal de Goiás (UFG)
Universidade Federal de Uberlândia (UFU)
Universidade Federal de São Paulo (UNIFESP)
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.
Language English
Sponsor Fundacao de Amparo a Pesquisa do Estado de Goias (FAPEG)
Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
Grant number Fundacao de Amparo a Pesquisa do Estado de Goias (FAPEG): 2012/0055431086
Fundacao de Amparo a Pesquisa do Estado de Goias (FAPEG): 2009/10267000352
CNPq: 477832/2010-5
CNPq: 483411/2012-4
Date 2014-10-03
Published in Plos One. San Francisco: Public Library Science, v. 9, n. 10, 10 p., 2014.
ISSN 1932-6203 (Sherpa/Romeo, impact factor)
Publisher Public Library Science
Extent 10
Origin http://dx.doi.org/10.1371/journal.pone.0109620
Access rights Open access Open Access
Type Article
Web of Science ID WOS:000342670800093
URI http://repositorio.unifesp.br/handle/11600/38321

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