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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

ESTRADIOL AND ANGIOTENSIN II CROSSTALK IN HYDROMINERAL BALANCE: ROLE OF THE ERK1/2 AND JNK SIGNALING PATHWAYS

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Author(s):
Almeida-Pereira, G. [1] ; Coletti, R. [1] ; Mecawi, A. S. [2] ; Reis, L. C. [2] ; Elias, L. L. K. [1] ; Antunes-Rodrigues, J. [1]
Total Authors: 6
Affiliation:
[1] Univ Sao Paulo, Sch Med Ribeirao Preto, Dept Physiol, BR-14049900 Ribeirao Preto - Brazil
[2] Univ Fed Rural Rio de Janeiro, Inst Biol, Dept Physiol Sci, BR-23890000 Seropedica - Brazil
Total Affiliations: 2
Document type: Journal article
Source: Neuroscience; v. 322, p. 525-538, MAY 13 2016.
Web of Science Citations: 6
Abstract

The angiotensin II (ANGII) receptor AT1 plays an important role in the control of hydromineral balance, mediating the dipsogenic and natriorexigenic effects and neuroendocrine responses of ANGII. While estradiol (E2) is known to modulate several actions of ANGII in the brain, the molecular and cellular mechanisms of the interaction between E2 and ANGII and its physiological role in the control of body fluids remain unclear. We investigated the influence of E2 (40 mu g/kg) pretreatment and extracellular-signal-regulated kinase (ERK1/2) and c-Jun N-terminal kinase (JNK) cell signaling on the dipsogenic and natriorexigenic effects, as well as the neuroendocrine responses to angiotensinergic central stimulation in ovariectomized rats (OVX). We showed that the inhibitory effect of E2 on ANGII-induced water and sodium intake requires the ERK1/2 and JNK signaling pathways. On the other hand, E2 pretreatment prevents the ANGII-induced phosphorylation of ERK and JNK in the lamina terminalis. E2 therapy decreased oxytocin (OT) and vasopressin (AVP) secretion and decreased ERK1/2 phosphorylation in the supraoptic and paraventricular nuclei (SON and PVN, respectively). We found that the AVP secretion induced by ANGII required ERK1/2 signaling, but OT secretion did not involve ERK1/2 signaling. Taken together, these results demonstrate that E2 modulates ANGII-induced water and sodium intake and AVP secretion by affecting the ERK1/2 and JNK pathways in the lamina terminalis and ERK1/2 signaling in the hypothalamic nuclei (PVN and SON) in OVX rats. (C) 2016 IBRO. Published by Elsevier Ltd. All rights reserved. (AU)

FAPESP's process: 12/04620-0 - Role of estradiol in thirst, sodium appetite and neuroendocrine responses induced by angiotensin II: Cellular mechanisms
Grantee:Gislaine de Almeida Pereira
Support Opportunities: Scholarships in Brazil - Doctorate