ANGIOTENSIN RECEPTOR NEPRILYSIN INHIBITOR LCZ696 ATTENUATES CARDIAC REMODELING IN EXPERIMENTAL MODEL OF METABOLIC SYNDROME

LAMA C; GARCIA RD; MIATELLO RM; GONZALEZ S; RENNA NF

Mendoza

Jornada; XXXIV Reunión Anual de la Sociedad de Biología de Cuyo; 2016

Sociedad Biología de Cuyo

ANGIOTENSIN RECEPTOR NEPRILYSIN INHIBITOR LCZ696 ATTENUATES CARDIAC REMODELING IN EXPERIMENTAL MODEL OF METABOLIC SYNDROMEGarcia R1, Gonzalez S1,2, Lama C1, Miatello R1,2, Renna NF1,21 Laboratoty of Cardiovascular Physiopathology IMBECU. CONICET. 2 Department of Pathology. School of Medicine. UNCuyo. E-mail: rodridg@hotmail.comHypertension and heart failure (HF) are major causes of death and morbidity in the Western world, and their prevalence is projected to increase. Increasing recognition that sustained overdrive of neurohormonal systems such as the renin?angiotensin?aldosterone system (RAAS) is involved in hypertension pathophysiology has led to the introduction of drugs inhibiting key components of the RAAS into clinical practice. The aim of this study was demonstrate the participation of LCZ969 (sacubitril valsartan; L) in cardiovascular remodeling. Methods: Male WKY and SHR were separated into five groups: Control, FFR: WKY rats receiving a 10% (w/v) fructose solution during all 12 weeks, SHR, FFHR: SHR receiving a 10% (w/v) fructose solution during all 12 weeks and FFHR+S: (68 mg/kg per day for 6 weeks) (n=8 each group). Metabolic variables and systolic blood pressure were measured. Cardiac remodelling was also evaluated. Results: L reverted an increase in systolic blood pressure but did not modify metabolic laboratory variables. Thus, chronic administration of L was able to revert cardiovascular hypertrophy. Conclusion: All these data suggest the involvement of RAAS and neprilysin system on the expression of different inflammatory and growth factors proteins in myocardial area, allowing the origination, perpetuation, amplification and destabilization of cardiovascular injury.