Central effect of angiotensin (1-7) on the vasopressin release during endotoxemic shock.

• Grant number: 15/09857-7
• Support Opportunities: Regular Research Grants
• Start date: October 01, 2016
• End date: September 30, 2018
• Field of knowledge: Biological Sciences - Physiology - General Physiology
• Principal Investigator: Evelin Capellari Cárnio
• Grantee: Evelin Capellari Cárnio
• Host Institution: Escola de Enfermagem de Ribeirão Preto (EERP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil

Abstract

The most widely accepted hypothesis to explain the biphasic response in the synthesis and release of vasopressin (AVP) observed during the change of homeostasis induced systemic inflammatory processes refers to the excessive production of inflammatory mediators. Among the main mediators there is the activation of the renin central angiotensin system (RAS) and the increase in pro-inflammatory cytokines, reactive oxygen species (ROS) and nitric oxide (NO). The synthesis of these inflammatory mediators may be adjusted by substances such as angiotensin II (ANG II), resulting in increased plasma AVP observed in the initial phase of endotoxemia model. However, excessive production of cytokines and ROS 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 its product, NO, during the late phase the endotoxêmico model. Overproduction of NO acts as an inhibitory factor in the synthesis of AVP, significantly reducing the plasma concentration of AVP. Addition to NO, the depletion of the stock of show AVP is an important mechanism contributing to the reduction of AVP. The angiotensin- (1-7) ((Ang- (1-7)), biologically active peptide angiotensinergic showed mediate endocrine effects similar to ANG II. However, unlike the ANG II, the Ang- (1-7) exerts antioxidant properties, anti-inflammatory, reducing ROS, pro-inflammatory cytokines, iNOS expression and NO concentration induced by administration of LPS. Therefore, the Ang- (1-7) shows a significant way to act as neuroprotective, receptor-mediated But in endotoxemia models. Therefore, the hypothesis of this project is that the administration of Ang- (1-7) can contribute reducing the pronounced fall in plasma AVP and prolonging the survival of animals exposed to LPS. (AU)

Scientific publications

(4)

(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, JAN 2021. (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, JUL 15 2020. (18/18459-3, 16/09364-3, 14/22477-6, 15/09857-7)

FAIM, FELIPE; PASSAGLIA, PATRICIA; BATALHAO, MARCELO; LACCHINI, RICCARDO; STABILE, ANGELITA MARIA; CARNIO, EVELIN CAPELLARI. Role of ghrelin on growth hormone/insulin-like growth factor-1 axis during endotoxemia. GROWTH HORMONE & IGF RESEARCH, v. 48-49, p. 36-44, OCT-DEC 2019. (15/09857-7, 16/17681-9)

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, AUG 2020. (11/20343-4, 15/09857-7, 14/22477-6)