Efferent pathways in sodium overload-induced renal vasodilation in rats.

Autor:	Amaral NO; Center for Neuroscience and Cardiovascular Physiology, Department of Physiological Sciences, Biological Sciences Institute, Federal University of Goiás, Goiânia, GO, Brazil., de Oliveira TS; Center for Neuroscience and Cardiovascular Physiology, Department of Physiological Sciences, Biological Sciences Institute, Federal University of Goiás, Goiânia, GO, Brazil., Naves LM; Center for Neuroscience and Cardiovascular Physiology, Department of Physiological Sciences, Biological Sciences Institute, Federal University of Goiás, Goiânia, GO, Brazil., Filgueira FP; Center for Neuroscience and Cardiovascular Physiology, Department of Physiological Sciences, Biological Sciences Institute, Federal University of Goiás, Goiânia, GO, Brazil., Ferreira-Neto ML; Faculty of Physical Education, Biological Sciences Institute, Universidade Federal de Uberlândia, Uberlândia, MG, Brazil., Schoorlemmer GH; Department of Physiology, Federal University of São Paulo, São Paulo, SP, Brazil., de Castro CH; Center for Neuroscience and Cardiovascular Physiology, Department of Physiological Sciences, Biological Sciences Institute, Federal University of Goiás, Goiânia, GO, Brazil., Freiria-Oliveira AH; Center for Neuroscience and Cardiovascular Physiology, Department of Physiological Sciences, Biological Sciences Institute, Federal University of Goiás, Goiânia, GO, Brazil., Xavier CH; Center for Neuroscience and Cardiovascular Physiology, Department of Physiological Sciences, Biological Sciences Institute, Federal University of Goiás, Goiânia, GO, Brazil., Colugnati DB; Center for Neuroscience and Cardiovascular Physiology, Department of Physiological Sciences, Biological Sciences Institute, Federal University of Goiás, Goiânia, GO, Brazil., Rosa DA; Center for Neuroscience and Cardiovascular Physiology, Department of Physiological Sciences, Biological Sciences Institute, Federal University of Goiás, Goiânia, GO, Brazil., Blanch GT; Center for Neuroscience and Cardiovascular Physiology, Department of Physiological Sciences, Biological Sciences Institute, Federal University of Goiás, Goiânia, GO, Brazil., Borges CL; Laboratory of Molecular Biology, Biological Sciences Institute, Federal University of Goiás, Goiânia, GO, Brazil., Soares CM; Laboratory of Molecular Biology, Biological Sciences Institute, Federal University of Goiás, Goiânia, GO, Brazil., Reis AA; Department of Biochemistry and Molecular Biology, Biological Sciences Institute, Federal University of Goiás, Goiânia, GO, Brazil., Cravo SL; Department of Physiology, Federal University of São Paulo, São Paulo, SP, Brazil., Pedrino GR; Center for Neuroscience and Cardiovascular Physiology, Department of Physiological Sciences, Biological Sciences Institute, Federal University of Goiás, Goiânia, GO, Brazil.
Jazyk:	angličtina
Zdroj:	PloS one [PLoS One] 2014 Oct 03; Vol. 9 (10), pp. e109620. Date of Electronic Publication: 2014 Oct 03 (Print Publication: 2014).
DOI:	10.1371/journal.pone.0109620
Abstrakt:	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 µg • 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 µg • 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.
Databáze:	MEDLINE
Externí odkaz:	Zobrazit plný text záznamu Plný text ve formátu PDF