Interaction of cellular mechanisms of estradiol and Angiotensin II in the central structures involved in the control of body fluids: in vitro study

• Grant number: 14/25005-8
• Support Opportunities: Scholarships in Brazil - Post-Doctoral
• Start date: June 01, 2015
• End date: May 31, 2019
• Field of knowledge: Biological Sciences - Physiology - Physiology of Organs and Systems
• Agreement: Coordination of Improvement of Higher Education Personnel (CAPES)
• Principal Investigator: José Antunes Rodrigues
• Grantee: Gislaine de Almeida Pereira
• Host Institution: Faculdade de Medicina de Ribeirão Preto (FMRP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil
• Associated scholarship(s): 17/22140-0 - A Novel Mechanism Controlling Neurohypophyseal Hormone Release, BE.EP.PD

Abstract

The renin-angiotensin system plays a fundamental role in controlling the homeostasis of bodily fluids, and angiotensin II (Ang II) as its main active hormone. The main effects exerted by ANG II in the control of electrolyte homeostasis, as dipsogenic, natriorexigenic and its neuroendocrine responses are mediated mainly by its AT1 receptor. It is known that this system is under the influence of the female hormones, especially estrogen (E2), which modulate the effects of ANG II mediated by the AT1 receptor. Recent data from our group have shown some of the interactions between the signaling pathways of E2 receptor and ANG II, and especially its physiological relevance in vivo studies. However, more studies on the cross-talk between signaling pathways of E2 receptor and ANG II are needed to elucidate the exact cellular mechanisms of interaction between these two hormones involved in the control of body fluids homeostasis. The elucidation of the components of the cascade of cellular signaling of the AT1 receptor and the estrogen receptor provides important information about the role of estrogens in physiological and pathophysiological conditions, such as dehydration and hypovolemia, modulating the effects of ANG II related with body fluids balance. In this context, the aim of this work is to investigate the cross-talk between estradiol and ANG II, mainly the MAPKs family proteins, protein kinase C and proteins involved with AT1 receptor dessensibilization, in response to angiotensinergic stimulation in organotypic cultures containing nucleus subfornical organ and hypothalamic paraventricular and supraoptic nuclei of female rats. (AU)

Scientific publications

(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)

ALMEIDA-PEREIRA, G.; VILHENA-FRANCO, T.; COLETTI, R.; COGNUCK, S. Q.; SILVA, H. V. P.; ELIAS, L. L. K.; ANTUNES-RODRIGUES. 17 beta-Estradiol attenuates p38MAPK activity but not PKC alpha induced by angiotensin II in the brain. Journal of Endocrinology, v. 240, n. 2, p. 345-360, FEB 2019. (13/09799-1, 14/25005-8)