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

Nathalia O Amaral,Thiago S De Oliveira,Gerard H M Schoorlemmer,Lara M Naves,Diego B Colugnati,Clayton L Borges,Gustavo R Pedrino,Graziela T Blanch,Angela A S Reis,Célia M A Soares,Carlos H De Castro,Fernando P Filgueira,André H Freiria-Oliveira,Marcos L Ferreira-Neto,Carlos H Xavier,Daniel A Rosa,Sergio L Cravo

doi:10.1371/journal.pone.0109620

Nathalia O Amaral, Thiago S De Oliveira + Show 15 more

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https://doi.org/10.1371/journal.pone.0109620

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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 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.

Highlights

Hypernatremia constitute a challenge that threatens the survival of the organism
OXTR gene expression in the renal artery The qRT-PCR analysis indicated that t OXTR was expressed in the renal artery (n = 10 arteries taken from 5 rats; Figure 1)
These findings demonstrated that OXTR gene was expressed as b-actin, a constitutive gene

Summary

Introduction

Hypernatremia constitute a challenge that threatens the survival of the organism. Despite the wide variation in daily intakes and losses of sodium, its concentration in the body fluids must be maintained within narrow limits. It is no surprise that multiple mechanisms are involved in the regulation of sodium concentration This wide variety of mechanism ranges from localized and highly specific renal control of sodium loss to the complex regulation of ingestive behaviors [3,4,5]. Changes in plasma sodium concentration trigger centrally driven behavioral and neurovegetative adjustments in order to correct deviations [3,4]. Hypertonicity reduces sympathetic renal nerve activity [5,6,7,8], induces renal vasodilatation [9,10,11,12], and increases release of vasopressin (VP), atrial natriuretic peptide (ANP) [13,14] and oxytocin (OT) [15,16,17,18] Together, these adjustments lead to natriuresis [19,20,21,22]

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