Efferent pathways in sodium overload-induced renal vasodilation in rats
Carregando...
Data
2014
Título da Revista
ISSN da Revista
Título de Volume
Editor
Resumo
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. kg21, 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 mg N kg21, 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 kg21 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 mg N kg21 N h21, 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.
Descrição
Palavras-chave
Citação
AMARAL, Nathalia O. et al. Efferent pathways in sodium overload-induced renal vasodilation in rats. Plos One, San Francisco, v. 9, n. 10, p. e109620, 2014.