Spontaneously hypertensive rats provide a model of genetic hypertension that allows the study of primary hypertension. The BIBW2992 EGFR/HER2 inhibitor administration of carbohydrate-rich diets to rats can induce insulin resistance, hyperinsulinemia, dyslipidemia and moderate hypertension. Chronic fructose-fed rats provide a useful GANT61 experimental model for studying the interaction of the factors that shape metabolic syndrome. We postulate that this dual experimental model could be appropriate for extrapolating results to human pathology. In the present study, 
we used vidagliptin to examine the role of the DDP-IV, incretin system component, in the activation of different molecular inflammatory cytokines, NF-kB and VCAM-1 to generate a microenvironment that supports cardiovascular remodeling. In this article, we demonstrated an important effect of DDP-IV in reducing vascular inflammation, accompanied by a favorable reduction in metabolic and structural parameters. The FFHR experimental model presents hypertension, dyslipidemia, insulin resistance, vascular and cardiac remodeling, inflammation demonstrated by increased hsCRP and vascular inflammation due to increased expression of NF-kB, VCAM-1 and pro-atherogenic cytokines. The increased expression of VCAM-1 is a marker of vascular inflammation, vascular permeability and endothelial dysfunction. The inflammatory process identified in this experimental model has two components: 1- a local component involving an increase in the levels of nuclear transcription factors with subsequent activation of the inflammatory cascade, resulting in a strong presence of cytokines, and level 2�C a systemic component involving increased hepatic synthesis of CRP due to a probable increase of IL-6. The data suggest that incretin system dysfunction, as happen in patients with diabetes mellitus or metabolic syndrome, allows activation of inflammatory response in different levels. With the consequent creation of a vascular microenvironment that is conducive to the creation, perpetuation, progression, and destabilization of vascular injury, with either a simple eutrophic mechanism of vascular remodeling, or the generation of an atherosclerotic lesion. A number of mechanisms may underlie these results. Given that GLP-1 is a physiological substrate of DPP-IV, DPP-IV inhibition by V may be expected to increase the circulating levels of GLP-1 Several studies have reported beneficial effects of GLP-1 on the cardiovascular system. In humans, Nikolaidis et al. have shown that a 72-h infusion of GLP-1 improved left ventricular function in patients with acute myocardial infarction and systolic dysfunction after successful reperfusion therapy, an effect that was observed in both diabetic and nondiabetic patients. The authors suggested that this observation might be explained by the insulinotropic and insulinomimetic properties of GLP-1; alternatively, GLP-1 might also improve endothelial function. Studies have shown that GLP-1 improves endothelium-dependent vascular responses in the brachial artery while leaving endotheliumindependent responses unaffected in healthy humans and patients with type 2 diabetes. The cardiovascular actions of GLP-1 may occur either directly through the GLP-1 receptor or through a GLP-1 receptor-independent effect of the degradation product of GLP-1, GLP-1. In addition to GLP-1, DPP-IV also degrades GIP, and potentially cytokines and certain chemokines. Thus, other substrates of DPP-IV may be responsible for the improvement in endothelial function. Alternatively, V might improve endothelial function by influencing insulin and glucose levels. Insulin causes vasodilatation by increasing endothelial production of NO.