| Autor: |
Passaglia P; Department of Physiology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, São Paulo 14049-900, Brazil., de Lima Faim F; Department of Physiology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, São Paulo 14049-900, Brazil., Batalhão ME; Department of General and Specialized Nursing, Ribeirão Preto College of Nursing, University of São Paulo, Ribeirão Preto, São Paulo 14040-902, Brazil., Stabile AM; Department of General and Specialized Nursing, Ribeirão Preto College of Nursing, University of São Paulo, Ribeirão Preto, São Paulo 14040-902, Brazil., Bendhack LM; Department of Physics and Chemistry, Faculty of Pharmaceutical Sciences of Ribeirão Preto, Ribeirão Preto-University of São Paulo, Ribeirão Preto, São Paulo 14040-903, Brazil., Antunes-Rodrigues J; Department of Physiology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, São Paulo 14049-900, Brazil., Lacchini R; Department of Psychiatric Nursing and Human Science, Ribeirão Preto College of Nursing, University of São Paulo, Ribeirão Preto, São Paulo 14040-902, Brazil., Capellari Carnio E; Department of General and Specialized Nursing, Ribeirão Preto College of Nursing, University of São Paulo, Ribeirão Preto, São Paulo 14040-902, Brazil. |
| Abstrakt: |
Angiotensin-(1-7) [Ang-(1-7)]/Mas receptor is a counter-regulatory axis that counteracts detrimental renin-angiotensin system (RAS) effects, especially regarding systemic inflammation, vasopressin (AVP) release, and hypothalamic-pituitary-adrenal (HPA) activation. However, it is not completely understood whether this system may control centrally or systemically the late phase of systemic inflammation. Thus, the aim of this study was to determine whether intracerebroventricular (i.c.v.) administration of Ang-(1-7) can modulate systemic inflammation through the activation of humoral pathways in late phase of endotoxemia. Endotoxemia was induced by systemic injection of lipopolysaccharide (LPS) (1.5 mg/kg, i.v.) in Wistar rats. Ang-(1-7) (0.3 nmol in 2 µL) promoted the release of AVP and attenuated interleukin-6 (IL-6) and nitric oxide (NO) levels but increased interleukin-10 (IL-10) in the serum of the endotoxemic rats. The central administration of Mas receptor antagonist A779 (3 nmol in 2 µL, i.c.v.) abolished these anti-inflammatory effects in endotoxemic rats. Furthermore, Ang-(1-7) applied centrally restored mean arterial blood pressure (MABP) without affecting heart rate (HR) and prevented vascular hyporesponsiveness to norepinephrine (NE) and AVP in animals that received LPS. Together, our results indicate that Ang-(1-7) applied centrally promotes a systemic anti-inflammatory effect through the central Mas receptor and activation of the humoral pathway mediated by AVP. |
