Renin-angiotensin intra-renal: inhibition of the renin activity of lipopolysaccharide of E. coli, in vivo

• Grant number: 09/03720-9
• Support Opportunities: Scholarships in Brazil - Scientific Initiation
• Effective date (Start): July 01, 2009
• Effective date (End): June 30, 2010
• Field of knowledge: Health Sciences - Medicine
• Principal Investigator: Waldemar Silva Almeida
• Grantee: Luciane Gomes Santana
• Host Institution: Departamento de Medicina. Escola Paulista de Medicina (EPM). Universidade Federal de São Paulo (UNIFESP). Campus São Paulo. São Paulo , SP, Brazil

Abstract

It is known that the LPS, the main structural component of toxic Gram-negative bacteria, is responsible for initiating the septic process causing imbalance in the production of vasodilator and vasoconstrictor substances that are responsible for systemic hemodynamic change and intra-renal by its direct action as a toxin on resident renal cells (mesangial and endothelial tubular epithelial). Mesangiais glomerular cells synthesize and are critically regulated by the action of various vasoactive hormones such as the platelet activating factor, Ang II, norepinephrine and endothelin, which respond by expression of active form in glomerular hemodynamics, forming the set of actions that help in performance of the activities undertaken by the SRA. The studies on SARS have been focused on the local assessment of their involvement with chronic kidney disease and its progression to the final stage, in diseases such as diabetic nephropathy and systemic effects that it triggers, especially the occurrence of ARF secondary to sepsis . And previously demonstrated that administration of LPS from E. Coli in rats caused a decrease in total GFR and individual (per unit néfron), linked by the increase in renal vascular resistance (PVR) and decrease in RPF. The Ang II, and functions in regulating glomerular hemodynamics, may be related to growth, differentiation and tissue repair, which once clearly defined, will be of great clinical support. (AU)