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Participation of angiotensin-(1-7) in the regulation of synthesis and release of vasopressin during endotoxemia

Grant number: 14/22477-6
Support Opportunities:Scholarships in Brazil - Doctorate
Start date: March 01, 2015
End date: August 31, 2019
Field of knowledge:Biological Sciences - Physiology - General Physiology
Agreement: Coordination of Improvement of Higher Education Personnel (CAPES)
Principal Investigator:Evelin Capellari Cárnio
Grantee:Patrícia Passaglia
Host Institution: Escola de Enfermagem de Ribeirão Preto (EERP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil
Associated scholarship(s):18/11464-1 - Ang-(1-7)/Mas and ET-1/ETR cross-talk in vascular smooth muscle cells: implications in vascular dysfunction in hypertension, BE.EP.DR

Abstract

The most widely accepted hypothesis to explain the biphasic response in the synthesis and release of vasopressin (AVP) observed during endotoxemia refers to the excessive production of inflammatory mediators. Among the main mediators highlights the central activation of the renin angiotensin system (RAS) and increased proinflammatory cytokines, reactive oxygen species (ROS) and nitric oxide (NO). The synthesis of these inflammatory mediators may be adjusted by substances such as angiotensin II (ANGII), resulting in the increase in plasma AVP observed in the initial stage of the endotoxemia model. However, excessive production of ROS and cytokines during the initial phase results in activation of transcription pathways that result in elevated expression of enzymes such as inducible nitric oxide synthase (iNOS) and of its product, NO, during the late phase endotoxêmico the model. Overproduction of NO acts as an inhibitory factor in the synthesis of AVP by reducing the plasma concentration of AVP. Addition to NO, depletion of the stock of AVP shown to be an important mechanism contributing to the reduction of plasma levels of AVP. The angiotensin-(1-7) ((Ang-(1-7)), angiotensinergic biologically active peptide, ANG II has been shown to mediate similar endocrine effects. However, different from ANG II to Ang-(1-7) exerts antioxidant properties, anti-inflammatory, reducing ROS, pro-inflammatory cytokines, iNOS expression and NO concentration induced by administration of LPS. Thus, the Ang-(1-7) could act as an important route neuroprotective, receptor-mediated but in models of endotoxemia. Hence, the hypothesis of this project is that administration of Ang-(1-7) may contribute to attenuating pronounced fall in plasma AVP and increasing survival of animals exposed to LPS. (AU)

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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)
PASSAGLIA, PATRICIA; DE LIMA FAIM, FELIPE; BATALHAO, MARCELO EDUARDO; STABILE, ANGELITA MARIA; BENDHACK, LUSIANE MARIA; ANTUNES-RODRIGUES, JOSE; LACCHINI, RICCARDO; CAPELLARI CARNIO, EVELIN. Central Administration of Angiotensin-(1-7) Improves Vasopressin Impairment and Hypotensive Response in Experimental Endotoxemia. CELLS, v. 10, n. 1, . (14/22477-6, 11/20343-4, 15/09857-7)
JESUS, ALINE A.; PASSAGLIA, PATRICIA; SANTOS, BRUNA M.; RODRIGUES-SANTOS, ISABELLE; FLORES, RAFAEL A.; BATALHAO, MARCELO E.; STABILE, ANGELITA M.; CARNIO, EVELIN C.. Chronic molecular hydrogen inhalation mitigates short and long-term memory loss in polymicrobial sepsis. Brain Research, v. 1739, . (18/18459-3, 16/09364-3, 14/22477-6, 15/09857-7)
PASSAGLIA, PATRICIA; FAIM, FELIPE DE LIMA; BATALHAO, MARCELO EDUARDO; BENDHACK, LUSIANE MARIA; ANTUNES-RODRIGUES, JOSE; ULLOA, LUIS; KANASHIRO, ALEXANDRE; CARNIO, EVELIN CAPELLARI. Central angiotensin-(1-7) attenuates systemic inflammation via activation of sympathetic signaling in endotoxemic rats. BRAIN BEHAVIOR AND IMMUNITY, v. 88, p. 606-618, . (11/20343-4, 15/09857-7, 14/22477-6)
Academic Publications
(References retrieved automatically from State of São Paulo Research Institutions)
PASSAGLIA, Patrícia. Central angiotensin-(1-7) effects on sympathetic efferent arc of inflammatory reflex in rats submitted to endotoxemia. 2019. Doctoral Thesis - Universidade de São Paulo (USP). Faculdade de Medicina de Ribeirão Preto (PCARP/BC) Ribeirão Preto.