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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.)

17 beta-Estradiol attenuates p38MAPK activity but not PKC alpha induced by angiotensin II in the brain

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Author(s):
Almeida-Pereira, G. [1] ; Vilhena-Franco, T. [1] ; Coletti, R. [1] ; Cognuck, S. Q. [1] ; Silva, H. V. P. [1] ; Elias, L. L. K. [1] ; Antunes-Rodrigues
Total Authors: 7
Affiliation:
[1] Sch Med Ribeirao Preto, Dept Physiol, Ribeirao Preto - Brazil
Total Affiliations: 1
Document type: Journal article
Source: Journal of Endocrinology; v. 240, n. 2, p. 345-360, FEB 2019.
Web of Science Citations: 0
Abstract

17 beta-Estradiol (E2) has been shown to modulate the renin-angiotensin system in hydromineral and blood pressure homeostasis mainly by attenuating angiotensin II (ANGII) actions. However, the cellular mechanisms of the interaction between E2 and angiotensin II (ANGII) and its physiological role are largely unknown. The present experiments were performed to better understand the interaction between ANGII and E2 in body fluid control in female ovariectomized (OVX) rats. Th e present results are the first to demonstrate that PKC/p38 MAPK signaling is involved in ANGII-induced water and sodium intake and oxytocin (OT) secretion in OVX rats. In a ddition, previous data from our group revealed that the ANGII-induced vasopressin (AVP) secretion requires ERK1/2 signaling. Therefore, taken together, the present observ ations support a novel concept that distinct intracellular ANGII signaling gives rise to distinct neurohypophyseal hormone release. Furthermore, the results show that E2 attenuat es p38 MAPK phosphorylation in response to ANGII but not PKC activity in th e hypothalamus and the lamina terminalis, suggesting that E2 modulates ANGII effects th rough the attenuation of the MAPK pathway. In conclusion, this work contributes to the f urther understanding of the interaction between E2 and ANGII signaling in hydromineral homeostasis, as well as it contributes to further elucidate the physiological relevance of PKC/p38 MAPK signaling on the fluid intake and neurohypophyseal release induced by ANGII. (AU)

FAPESP's process: 13/09799-1 - Energy balance and body fluid homeostasis control: from cells to the physiological systems
Grantee:José Antunes Rodrigues
Support Opportunities: Research Projects - Thematic Grants
FAPESP's process: 14/25005-8 - Interaction of cellular mechanisms of estradiol and Angiotensin II in the central structures involved in the control of body fluids: in vitro study
Grantee:Gislaine de Almeida Pereira
Support Opportunities: Scholarships in Brazil - Post-Doctoral