PROINFLAMMATORY CITOKINS IN VASCULAR REMODELING OF METABOLIC SYNDROME MODEL

RENNA NF; ASTESIANO A; GONZALEZ S; LAMA C; MIATELLO RM

Belo Horizaonte, Brazil

Congreso; XVII Congresso Brasileiro de Hipertensão / IASH 2009; 2009

Inter-american society of Hypertension and Sociedad Brasileira de Hipertensão

The inflammation more and more carries out an important roll in vascular remodeling and atherogenesis especially in the metabolic syndrome. The citokins are a category of proteins and glycoproteins, act as of intercellular communication. They can be classified like lynfokins, interleukins or quimokins. The expression of inflammatory markers in the arterial wall has been demonstrated previously in an experimental model of metabolic syndrome (MS) in rats.  Vascular remodeling is characterized by wall hypertrophy and reduction in the L/M ratio, mediated by the synthesis and release of vasoactive and growth factors, in this experimental model could be demonstrated: increased cascade of growth factors, product of insulin resistance and vascular inflammation by expression of NF-¦ÊB and VCAM-1, added to hypertrophy caused by sustained hypertension. The objective was to examine the participation of proinflammatory citokins in physiopathology of vascular remodeling associate to metabolic syndrome WKY and SHR male distributed in 4 groups: 1- WKY; 2- FFR: WKY + fructose in water drink at 10% during 12 week; 3- SHR and 4-  FFHR: SHR + fructose in water drink at 10% during 12 week When finalizing the protocols was examined: Sistolic Blood pressure (SBP), Fast glycemia, triglyceridemia (TG), colesterol total and colesterol-HDL (c-HDL), insulin, HOMA index,  C reactive preotein high-sensitive (CRP-hs), cardiac hypertrophy by relative heart weight and myocardiocyte area, Lumen/media (L/M) ratio, expression of citokins by comercial ChemiArray system (rat antibody arrays): CINC-2, CINC-3, CX3CL1, CNTF, MCP-1, MIP-3¦Á, ¦Â-NGF, TIMP-1, VEGF, GM-CSF, INF-¦Ã, IL-1¦Á,  IL-1¦Â, IL-4, IL-6, IL-10, LIX, Leptin and TNF-alfa Data (media¡Àsem) were processed by ANOVA and post-test de Bonferroni (*p<0.001 v WKY y #p<0.001 v FFHR). The data confirm the development of the experimental model and suggest the participation of genes promoters that participate in the pathological model, which in addition they are involved in development of cardiac and vascular remodeling present in the metabolic syndrome. The data contribute to sustain the hypothesis that suggests the participation of the local and sist¨¦mico inflammatory process the associated process of remodelado vascular to this experimental model.